Helicobacter pylori infection: A balance between bacteria and host

array:24 ["pii" => "S0325754122000347" "issn" => "03257541" "doi" => "10.1016/j.ram.2022.04.003" "estado" => "S300" "fechaPublicacion" => "2023-01-01" "aid" => "500" "copyright" => "Asociación Argentina de Microbiología" "copyrightAnyo" => "2022" "documento" => "article" "crossmark" => 1 "licencia" => "http://creativecommons.org/licenses/by-nc-nd/4.0/" "subdocumento" => "fla" "cita" => "Rev Argent Microbiol. 2023;55:60-7" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:1 [ "total" => 0 ] "itemSiguiente" => array:19 [ "pii" => "S0325754122000578" "issn" => "03257541" "doi" => "10.1016/j.ram.2022.06.001" "estado" => "S300" "fechaPublicacion" => "2023-01-01" "aid" => "508" "copyright" => "Asociación Argentina de Microbiología" "documento" => "article" "crossmark" => 1 "licencia" => "http://creativecommons.org/licenses/by-nc-nd/4.0/" "subdocumento" => "fla" "cita" => "Rev Argent Microbiol. 2023;55:68-72" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:1 [ "total" => 0 ] "en" => array:14 [ "idiomaDefecto" => true "cabecera" => "Brief report" "titulo" => "Bloodstream infection by Rhodococcus corynebacterioides in a pediatric patient diagnosed with high-risk retinoblastoma" "tienePdf" => "en" "tieneTextoCompleto" => "en" "tieneResumen" => array:3 [ 0 => "en" 1 => "en" 2 => "es" ] "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "68" "paginaFinal" => "72" ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Infección del torrente sanguíneo por Rhodococcus corynebacterioides en un paciente pediátrico con diagnóstico de retinoblastoma de alto riesgo" ] ] "contieneResumen" => array:2 [ "en" => true "es" => true ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 937 "Ancho" => 1675 "Tamanyo" => 67641 ] ] "descripcion" => array:1 [ "en" => "Maximum likelihood phylogenetic tree showing the taxonomic affiliation of the strain isolated from the blood samples (accession number MH458891). The tree was constructed with 16S rDNA gene sequences. Numbers at nodes represent the percentages of occurrence of nodes in 1000 bootstrap trials. The 16S rDNA gene from Microbacterium barkeri strain served as outgroup." ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Ana Rosa Méndez-Cruz, Georgina Elizabeth Félix-Bermúdez, Dinora Virginia Aguilar-Escobar, Lourdes Vega-Vega, Aurea Itzel Morales-Estrada, Araceli Contreras-Rodríguez" "autores" => array:6 [ 0 => array:2 [ "nombre" => "Ana Rosa" "apellidos" => "Méndez-Cruz" ] 1 => array:2 [ "nombre" => "Georgina Elizabeth" "apellidos" => "Félix-Bermúdez" ] 2 => array:2 [ "nombre" => "Dinora Virginia" "apellidos" => "Aguilar-Escobar" ] 3 => array:2 [ "nombre" => "Lourdes" "apellidos" => "Vega-Vega" ] 4 => array:2 [ "nombre" => "Aurea Itzel" "apellidos" => "Morales-Estrada" ] 5 => array:2 [ "nombre" => "Araceli" "apellidos" => "Contreras-Rodríguez" ] ] ] ] "resumen" => array:1 [ 0 => array:3 [ "titulo" => "Highlights" "clase" => "author-highlights" "resumen" => "<ul class="elsevierStyleList" id="lis0005"><li class="elsevierStyleListItem" id="lsti0005">•R. corynebacterioides is considered as an opportunistic pathogen in humans.</li><li class="elsevierStyleListItem" id="lsti0010">•R. corynebacterioides is underestimated as cause of bacteremia in cancer patients.</li><li class="elsevierStyleListItem" id="lsti0015">•16S rRNA sequence analysis confirmed the identification of R. corynebacterioides.</li></ul>" ] ] ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0325754122000578?idApp=UINPBA00004N" "url" => "/03257541/0000005500000001/v1_202303161058/S0325754122000578/v1_202303161058/en/main.assets" ] "itemAnterior" => array:19 [ "pii" => "S0325754122000335" "issn" => "03257541" "doi" => "10.1016/j.ram.2022.02.007" "estado" => "S300" "fechaPublicacion" => "2023-01-01" "aid" => "499" "copyright" => "Asociación Argentina de Microbiología" "documento" => "article" "crossmark" => 1 "licencia" => "http://creativecommons.org/licenses/by-nc-nd/4.0/" "subdocumento" => "fla" "cita" => "Rev Argent Microbiol. 2023;55:49-59" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:1 [ "total" => 0 ] "en" => array:14 [ "idiomaDefecto" => true "cabecera" => "Original article" "titulo" => "Seroprevalence of human leptospirosis in a rural community from Tandil, Argentina. Assessment of risk factors and spatial analysis" "tienePdf" => "en" "tieneTextoCompleto" => "en" "tieneResumen" => array:3 [ 0 => "en" 1 => "en" 2 => "es" ] "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "49" "paginaFinal" => "59" ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Seroprevalencia de leptospirosis humana en una comunidad rural del partido de Tandil (Argentina). Identificación de los factores de riesgo y del análisis espacial" ] ] "contieneResumen" => array:2 [ "en" => true "es" => true ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0010" "etiqueta" => "Figure 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 1224 "Ancho" => 1340 "Tamanyo" => 333313 ] ] "descripcion" => array:1 [ "en" => "Spatial clusters detected with higher risk of infection with Leptospira spp., and of the presence of the main risk factors." ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Julia A. Silva, Exequiel A. Scialfa, Matías Tringler, Marcelo G. Rodríguez, Adela Tisnés, Santiago Linares, Mariana A. Rivero" "autores" => array:7 [ 0 => array:2 [ "nombre" => "Julia A." "apellidos" => "Silva" ] 1 => array:2 [ "nombre" => "Exequiel A." "apellidos" => "Scialfa" ] 2 => array:2 [ "nombre" => "Matías" "apellidos" => "Tringler" ] 3 => array:2 [ "nombre" => "Marcelo G." "apellidos" => "Rodríguez" ] 4 => array:2 [ "nombre" => "Adela" "apellidos" => "Tisnés" ] 5 => array:2 [ "nombre" => "Santiago" "apellidos" => "Linares" ] 6 => array:2 [ "nombre" => "Mariana A." "apellidos" => "Rivero" ] ] ] ] "resumen" => array:1 [ 0 => array:3 [ "titulo" => "Highlights" "clase" => "author-highlights" "resumen" => "<ul class="elsevierStyleList" id="lis0005"><li class="elsevierStyleListItem" id="lsti0005">•Epidemiologic and spatial analysis of leptospirosis can be applied in human population.</li><li class="elsevierStyleListItem" id="lsti0010">•Information about leptospirosis in rural areas is scarce.</li><li class="elsevierStyleListItem" id="lsti0015">•Preventive measures can be applied for human leptospirosis from rural areas.</li></ul>" ] ] ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0325754122000335?idApp=UINPBA00004N" "url" => "/03257541/0000005500000001/v1_202303161058/S0325754122000335/v1_202303161058/en/main.assets" ] "en" => array:21 [ "idiomaDefecto" => true "cabecera" => "Original article" "titulo" => "Helicobacter pylori infection: A balance between bacteria and host" "tieneTextoCompleto" => true "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "60" "paginaFinal" => "67" ] ] "autores" => array:1 [ 0 => array:4 [ "autoresLista" => "Pamela Bucci, Yanina Barbaglia, Fabián Tedeschi, Fabián Zalazar" "autores" => array:4 [ 0 => array:3 [ "nombre" => "Pamela" "apellidos" => "Bucci" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "a" "identificador" => "aff0005" ] ] ] 1 => array:3 [ "nombre" => "Yanina" "apellidos" => "Barbaglia" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "b" "identificador" => "aff0010" ] ] ] 2 => array:3 [ "nombre" => "Fabián" "apellidos" => "Tedeschi" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "a" "identificador" => "aff0005" ] ] ] 3 => array:4 [ "nombre" => "Fabián" "apellidos" => "Zalazar" "email" => array:1 [ 0 => "fzalazar@fbcb.unl.edu.ar" ] "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "*" "identificador" => "cor0005" ] ] ] ] "afiliaciones" => array:2 [ 0 => array:3 [ "entidad" => "Laboratorio de Práctica Profesional de Bioquímica, Facultad de Bioquímica y Ciencias Biológicas, Universidad Nacional del Litoral, Subsuelo Hospital “Dr. José María Cullen”, Avda. Freyre 2150, (S3000EOZ) Santa Fe, Argentina" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Servicio de Gastroenterologia, Subsuelo Hospital “Dr. José María Cullen”, Avda. Freyre 2150 (S3000EOZ) Santa Fe, Argentina" "etiqueta" => "b" "identificador" => "aff0010" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Helicobacter pylori: un balance entre bacterias y huésped" ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1270 "Ancho" => 1673 "Tamanyo" => 114120 ] ] "descripcion" => array:1 [ "en" => "Frequency of H. pylori genotypes in patients with chronic gastritis presenting different histological findings. (1) cagA(+); (2) vacAs1m1; (3) vacAs1m2; (4) vacAs2m1; (5) vacAs2m2; (6) babA2; (7) cagA(+)/vacAS1M1; (8) cagA(+)/vacAS1M1/babA2(+)." ] ] ] "textoCompleto" => "IntroductionHelicobacter pylori (H. pylori) is a gastric pathogen widely recognized as a causative agent of gastritis worldwide. Furthermore, H. pylori is an important etiological agent for a multi-step cascade which, starting from chronic gastritis, can evolve to pre-neoplastic lesions (such as intestinal metaplasia), dysplasia and up to gastric adenocarcinoma<a class="elsevierStyleCrossRefs" href="#bib0325">10,15,17,46,52</a>. In fact, in 1994 it has been classified as a Class I carcinogen by the International Agency for Research on Cancer<a class="elsevierStyleCrossRef" href="#bib0365">18</a>. In addition, gastric cancer remains the 3rd leading cause of cancer-related death and the leading cause of infection-related cancer worldwide<a class="elsevierStyleCrossRef" href="#bib0335">12</a>. Epidemiology of gastric cancer shows a high variability: there are countries presenting high prevalence (e.g., Korea, Japan, China, Colombia, Chile) whereas others show low prevalence rates (generally, developed countries such as USA, Canada and Australia). Infection rates in Argentina are found at intermediate values, with the highest values as well as the highest mortality rate from stomach cancer reported in the southern provinces<a class="elsevierStyleCrossRefs" href="#bib0330">11,12,25,27,37</a>.It has been mentioned that the cascade of events that would lead to adenocarcinoma seems to be triggered – among other causes – by bacterial-specific virulence factors (such as the cagA, vacA, babA2 gene) as well as by factors such as polymorphisms in cytokine genes<a class="elsevierStyleCrossRefs" href="#bib0320">9,21,43,50</a>. In this sense, greater mucosal Interleukin 6 (IL-6) levels in early gastric cancer with active H. pylori infection than those without H. pylori infection49, have been observed. In addition, individuals with the G allele at position -174 in the promoter sequence of IL-6 have been shown to produce higher levels of IL-6<a class="elsevierStyleCrossRef" href="#bib0340">13</a>. More recently, the importance of IL-6 mediated stromal–epithelial cell interaction in gastric tumorigenesis has been suggested<a class="elsevierStyleCrossRef" href="#bib0385">22</a>.The abovementioned Correa's cascade is often referred to follow a linear progression; nevertheless, most patients present little or no change over time. On the contrary, other patients exhibiting a dynamic process alternating regression and/or progression of lesions in their gastric mucosa and even rapid progression bypassing some of the putative steps is not an infrequent finding. It has been suggested that intestinal metaplasia (IM) is a “point of no return”, at which eradication is less effective at causing regression and indeed does not change the risk of progression in certain patients: once IM is established, eradication of H. pylori only partially achieves a successful reduction of the risk of progression to adenocarcinoma and the genetic damage to gastric stem cells becomes irreversible<a class="elsevierStyleCrossRef" href="#bib0390">23</a>.In Argentina, despite the important studies carried out in relation to the prevalence of infection and resistance of H. pylori to the different antibiotics used for its eradication<a class="elsevierStyleCrossRefs" href="#bib0295">4,19,20,34,35,48,53</a> there are no reports simultaneously analyzing a profile of virulence factors of the bacterium and polymorphisms in cytokine genes of the host in patients with chronic gastritis showing different histopathological findings in the gastric mucosa (including pre-neoplastic lesions such as intestinal metaplasia). Hence, our aim was to begin an evaluation of H. pylori genotypes in adult patients residing in the north-central region of the Province of Santa Fe (Argentina) with different degrees of chronic gastritis, along with SNP-174 G>C in the promoter sequence of the IL-6 gene.Material and methodsPatients and samples. Adult dyspeptic patients (n=270) attending the Gastroenterology Service of “Dr. José María Cullen” Hospital (Santa Fe, Argentina) were enrolled in the study after informed consent was obtained. All of them underwent upper gastrointestinal endoscopy. The study was approved by the Research Ethics Advisory Committee of the Facultad de Bioquímica y Ciencias Biológicas (Universidad Nacional del Litoral) as well as by the Ethics Committee of the “Hospital Dr. J.M. Cullen”. Patients who had received antibiotic therapy and/or PPIs in the last 15 days were excluded from the study. Both biopsy sampling and histological analyses were carried out following the modified Sydney standardized protocol. Activity of gastritis was defined by the presence of neutrophils in the gastric mucosa. Two additional samples were taken from antrum and corpus for the rapid urease test and molecular detection of H. pylori.DNA purification and H. pylori molecular detection. DNA purification was carried out following a procedure using Proteinase K as previously described<a class="elsevierStyleCrossRef" href="#bib0295">4</a>. DNA integrity was evaluated by agarose gel electrophoresis; DNA yields and purity were assessed by absorbance analysis at 260/280nm. Purified DNA was stored at −20°C until use. H. pylori was studied in gastric biopsies by nested PCR targeting the hsp60 gene, using previously reported conditions<a class="elsevierStyleCrossRef" href="#bib0375">20</a>.H. pylori cagA, vacA and babA2 gene analysis. cagA, vacA and babA2 genes were analyzed by multiplex PCR using sequence specific primers<a class="elsevierStyleCrossRef" href="#bib0295">4</a>.Analysis of -174 G>C single nucleotide polymorphism (SNP) in the IL-6 gene. The SNP-174 G>C (rs1800795) in the promoter sequence of the IL-6 gene was analyzed by PCR-RFLP according to Guzman-Guzman et al<a class="elsevierStyleCrossRef" href="#bib0355">16</a>. As a control, the same SNPs were also analyzed in a group of H. pylori (−) patients. In all cases, the -174 G>C IL-6 polymorphism was in Hardy–Weinberg equilibrium, which was similar to that recently reported by Strauss et al.<a class="elsevierStyleCrossRef" href="#bib0500">45</a>, when evaluating the distribution of IL-6 genotypes in seronegative and seropositive Argentine individuals for Chagas diseaseAgarose gel electrophoresis. PCR products were analyzed by electrophoresis in 2% agarose gels (D1 Agarose, Biodynamics, Argentina). All in vitro amplification reactions included an internal control (human beta-globin gene). PCR-RFLP fragments were resolved in 3% agarose gels (LE Agarose, Inbio Highway, Argentina). All gels were prepared in the presence of a fluorescent stain and photographed under UV light.Statistical analysis. The association between categorical variables was evaluated using the Chi-square test and Odds ratio. A p-value <0.05 was considered statistically significant. A Hardy–Weinberg equilibrium analysis was carried out to evaluate the -174 G>C polymorphism in the IL-6 gene.ResultsThe analysis was performed on samples from 132 patients with a histological diagnosis of chronic gastritis and with positive results for H. pylori by in vitro amplification of the hsp60 gene plus histological analysis and/or rapid urease test (in other words, if a positive result was obtained by 2 out of 3 tests).The age range of patients was 18–65 years, with a mean value of 41.7 years (median=41). With regard to gender, 68.1% (90) and 31.8% (42) were women and men, respectively, in a 2.14:1 ratio.When analyzing the H. pylori genotypes present, the presence of the cagA gene was detected in 34% of all patients with chronic gastritis, while the babaA2 gene was present in 53% of the samples analyzed.All patients presented the vacA gene in its different variants: 67% corresponded to the m1s1 variant, followed by the m2s2 and m2s1 variants, in 25% and 8%, respectively; the presence of the vacAS2M1 variant was not detected. The cagA(+)/vacA m1s1 combination (reported as one of the most virulent) was found in 32% of the patients, while the genotype called “triple virulent” cagA(+)/vacAm1s1/babA2 (+) was present in 18% of patients.Taking into account the alterations in the gastric mucosa, the total number of patients was reclassified into 3 groups (a) patients with inactive chronic gastritis (ICG, n=43; age: mean, 41.4; range=18–65), (b) patients with active chronic gastritis without intestinal metaplasia (ACGIM−, n=69; age: mean, 40.3; range=22–60) and (c) patients with active chronic gastritis with intestinal metaplasia (ACGIMI+, n=20; age: mean, 46.3; range=28–64). No significant differences were found in relation to the age of the different groups (p>0.05).When analyzing the distribution of H. pylori genotypes in the 3 above-mentioned groups, although there were no significant differences between them, interestingly the group of ACGIM+ patients exhibited the highest proportion of genotypes cagA(+), vacAs1m1 and the combination cagA(+)/vacAm1s1 as well as the highest proportion of the “triple virulent” genotype cagA(+)/vacAm1s1/babA2.On the contrary, although the ICG group showed the highest frequency of babA2 (+) strains, it also had the lowest frequency of cagA(+), vacAs1m1 genotypes and the cagA(+)/vacAm1s1 and cagA(+) combinations/vacAm1s1/babA2 (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>).<elsevierMultimedia ident="fig0005"></elsevierMultimedia>Then, the -174 G>C polymorphism in the promoter sequence of the IL-6 gene was analyzed in each group. Based on our results, the ACGIM+ group showed the highest proportion of both the high-expression GG haplotype and the G allele, with significant differences compared to the ICG group (p<0.05).Finally, the -174 G>C polymorphism in the IL-6 gene was analyzed in conjunction with the H. pylori genotypes present in each group. In this case, in the group of patients with ACGIM+ we found the highest proportion of cagA(+)/IL-6 GG, cagA(+)/vacAm1s1/IL-6GG and cagA(+)/vacAm1s1/babA2 (+)/IL-6GG combinations, with significant differences both with the ICG group and with the patients with ACGIM− (p<0.05) (<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>).<elsevierMultimedia ident="tbl0005"></elsevierMultimedia>Furthermore, there was 4–5 times greater probability of finding patients exhibiting the GG genotype for SNP -174 G>C IL-6, which in turn were infected with the most virulent H. pylori genotypes – cagA(+),cagA(+)/vacAm1s1 and cagA(+)/vacAm1s1/babA2 – in the ACGIM+ group in comparison to the patients of the ICG group (<a class="elsevierStyleCrossRef" href="#tbl0010">Table 2</a>).<elsevierMultimedia ident="tbl0010"></elsevierMultimedia>DiscussionThe association between H. pylori infection and gastric cancer is a well-known clinical event. Moreover, H. pylori is recognized as one of the factors that would contribute to the development of the cascade of events described by Correa<a class="elsevierStyleCrossRef" href="#bib0325">10</a>, which begins with chronic gastritis followed by the development of pre-neoplastic lesions (such as intestinal metaplasia) leading to adenocarcinoma<a class="elsevierStyleCrossRef" href="#bib0435">32</a>. On the other hand, different articles have shown important differences in relation to the infecting H. pylori genotypes as well as the epidemiology of gastric cancer around the world and even within the same country<a class="elsevierStyleCrossRefs" href="#bib0300">5,8,38,47,55</a>. Furthermore, different studies have explored the role of polymorphisms in interleukins associated with pre-neoplastic lesions in patients infected with H.pylori<a class="elsevierStyleCrossRefs" href="#bib0485">42,54</a>.In this context, our country has a vast surface area and although important studies in relation to the prevalence of infection as well as resistance to antibiotics have been published<a class="elsevierStyleCrossRefs" href="#bib0295">4,19,20,34,35,48,53</a>, to our knowledge there are no studies that simultaneously analyze: (a) the profile of virulence factors of the bacterium, (b) the polymorphisms in the cytokine genes of patients with chronic gastritis and (c) the histopathological findings in the gastric mucosa, including pre-neoplastic lesions such as intestinal metaplasia. Taking this into account, our aim was to begin a study focused on these variables in adult patients with chronic gastritis from the north-central region of Santa Fe province (Argentina).Based on our results, the frequency of the best-studied virulence factors (cagA, vacA and babA2) in patients with chronic gastritis is related to previous studies in Argentina<a class="elsevierStyleCrossRefs" href="#bib0305">6,24,26,28,31,48</a>. However, some differences can be highlighted: the frequency of the cagA gene found in our study (34%) is similar to that reported in the western region (30–40.8%)<a class="elsevierStyleCrossRefs" href="#bib0415">28,48</a>; however, lower than the data for Buenos Aires city (71–84%)<a class="elsevierStyleCrossRefs" href="#bib0305">6,24,26</a>. On the other hand, as reported by other authors in our country, the vacAm1s1 variant was predominant in the group of patients with chronic gastritis studied<a class="elsevierStyleCrossRefs" href="#bib0305">6,24,28,48</a>. With respect to the virulence factor babA2, we found a considerably higher proportion of patients carrying this gene than that reported by Medina et al.<a class="elsevierStyleCrossRef" href="#bib0430">31</a>, who found 9.7% in gastric biopsies of patients from another geographical region of our country. This could represent a real difference in the circulating genotypes or might be due to different experimental conditions, fundamentally given by the sequence of primers used for the amplification of the babA2 gene, as recently indicated<a class="elsevierStyleCrossRef" href="#bib0495">44</a>, as well as by the presence of allelic variations in the babA2 gene owing to microevolution phenomena described during colonization in some patients<a class="elsevierStyleCrossRef" href="#bib0420">29</a>. This microheterogeneity has been reported previously in interesting studies by Matteo et al.<a class="elsevierStyleCrossRef" href="#bib0425">30</a> and Armitano et al.<a class="elsevierStyleCrossRef" href="#bib0280">1</a> where the cag pathogenicity island (cagPAI), vacA, bab, oipA, dupA status and the presence of several genes from the genomic plasticity zone were studied to analyze intra-host variation in patients with chronic gastritis and peptic ulcer disease. In these studies, an inter-niche variability was proven for most of the genes analyzed in the cagPAI, for the genes oipA, dupA and for those in the plasticity region and, in a lesser extent, for the bab gene. However, such significant variability was not observed for the cagA and vacA genes. Matteo et al.<a class="elsevierStyleCrossRef" href="#bib0425">30</a> found that 37/40 patients had isolates with the same profile for the vacA gene whereas Armitano et al.<a class="elsevierStyleCrossRef" href="#bib0280">1</a>, identified that 24/28 and 25/28 patients had H. pylori isolates with the same status for the cagA and vacA genes respectively, in the different niches studied.In the next analysis, when classifying the patients into groups according to the histological findings (inactive chronic gastritis, active chronic gastritis IM− and active chronic gastritis IM+), as expected, we observed a trend towards a higher proportion of patients carrying the most virulent genotypes in patients with active chronic gastritis IM+, although differences were not statistically significant. However, when the analysis of the -174 G>C SNP in the IL-6 gene was included, we found a higher proportion of the IL-6 GG genotype in patients infected with both cagA(+) H. pylori strains as well as with the combinations cagA(+)/vacAs1m1 and cagA+/vacAs1m1/babA2 (+) in the active chronic gastritis IM+ group in relation to the other two groups. In this case, differences were significant in patients with inactive chronic gastritis as well as in patients with active chronic gastritis that did not exhibit intestinal metaplasia.Previous studies were conducted to analyze the impact of polymorphisms at position -174 of the IL-6 promoter in the development of gastric pathologies in the presence of H. pylori, with contradictory results. Similarly to our study, Gatti et al.<a class="elsevierStyleCrossRef" href="#bib0345">14</a> found an association between the GG alleles of IL-6 (-174 base) and the presence of gastric adenocarcinoma, independently of the tumor type (diffuse or intestinal). Similarly, a study conducted in Portugal reported a higher frequency of the IL-6 -174C/G genotype in the gastric cancer cases analyzed<a class="elsevierStyleCrossRef" href="#bib0475">40</a>. Attar et al.<a class="elsevierStyleCrossRef" href="#bib0285">2</a> also found a high frequency of the G allele and the GG genotype in patients compared to control subjects, suggesting that the polymorphism could influence the susceptibility to gastric cancer. On the other hand, although our findings differ from those by Ramis et al.<a class="elsevierStyleCrossRef" href="#bib0455">36</a> and Santos et al.<a class="elsevierStyleCrossRef" href="#bib0480">41</a> who found no correlation between polymorphisms in IL-6 and a higher risk of gastric carcinoma, they are consistent with the possibility of finding greater lesions in the gastric mucosa of those patients infected with more virulent strains of H. pylori with a potential higher local inflammatory response triggered by a greater expression of pro-inflammatory cytokines such as IL-6. In this sense, individuals with the G allele at position -174 have been shown to produce higher levels of IL-6<a class="elsevierStyleCrossRef" href="#bib0340">13</a>. Furthermore, mucosal IL-6 levels were also greater in early gastric cancer with active H. pylori infection than without H. pylori infection, and the levels decreased dramatically after the eradication of infection<a class="elsevierStyleCrossRef" href="#bib0520">49</a>. In a similar way, a positive correlation between mucosal IL-6 mRNA expression level and virulence factors of H. pylori in Iranian adult patients with chronic gastritis has been recently reported<a class="elsevierStyleCrossRef" href="#bib0290">3</a>. In addition, Kinoshita et al.<a class="elsevierStyleCrossRef" href="#bib0385">22</a>, among other authors, suggested the importance of IL-6 mediated stromal–epithelial cell interaction in gastric tumorigenesis.Due to the fact that Latin America is a region with one of the highest mortality rates due to gastric cancer in the world<a class="elsevierStyleCrossRef" href="#bib0310">7</a> and since it has been mentioned that, in some individuals, intestinal metaplasia might be a “point of no return” to the development of gastric adenocarcinoma, we consider relevant to report the first analysis in our region (Santa Fe, Argentina) of H. pylori genotypes and IL-6 SNP in patients with different types of gastritis, including pre-neoplastic lesions such as intestinal metaplasia. It should be noted that our analysis not only included the presence/absence of H. pylori associated to gastritis and pre-neoplastic alterations but also the identification of H. pylori genotypes along with the -174 G>C polymorphism on the IL-6 gene in each patient.These results obtained so far for our region would be in accordance with the idea that the transition towards more severe alterations during H. pylori infection would result from a balance between specific factors of the bacterium and host factors that modulate the inflammatory response during infection of the gastric mucosa.In this sense, a recent review by Rudnicka et al.<a class="elsevierStyleCrossRef" href="#bib0470">39</a> analyzed results from large-scale epidemiological studies, literature meta-analyses as well as from clinical and animal model studies focusing on the search of host immune system regulators (such SNPs in cytokines/growth factors) together with H. pylori virulence factors that facilitate the development of pre-cancerous and cancerous lesions, in the context of environmental and geographical determinants. Among the bacterial determinants related to gastric cancer development, they highlighted the infection with cagA-positive (particularly with a high number of EPIYA-C phosphorylation motifs) and vacA-positive isolates (in particular s1/m1 allele strains). They also reported that the combined genotyping of bacterial and host determinants suggests that the accumulation of polymorphisms favoring host and bacterial features increases the risk for precancerous and cancerous lesions in patients and they also suggested that biological determinants are urgently needed to predict the clinical course of infection in individuals with confirmed H. pylori infection.Furthermore, a whole-genome analysis was recently used to study 723 H. pylori genomes from different regions of the world in order to compare American (from 14 geographical sites across America, from Canada to Argentina) versus non-American populations<a class="elsevierStyleCrossRef" href="#bib0440">33</a>. In this study, genetic variants that were more common in the Americas than in the populations from other continents were identified, mainly resulting in non-synonymous mutations in functionally relevant regions of virulence genes (among them, cagA, vacA and babA genes), in domains known to interact with molecules of the host. Based on previous reports, it was suggested that the progression to serious clinical diseases, such as gastric cancer, is associated with the carriage of specific genotypes of the bacterium, in particular those that carry genes linked with virulence, concluding that the differences found between American and non-American H. pylori genomes could reflect a co-evolutionary process potentially contributing to the high risk of gastric cancer in the region.To date, our work has aimed at analyzing the presence or absence of the most studied genes in H. pylori (cagA, vacA and babA2) and their association with the severity of gastric lesions without considering variations in their structure (such as those due to the presence of different types/number of EPIYA sequences), additional polymorphisms in the cagA gene or the integrity of cag PAI which mediates efficient CagA translocation, important for the commencement of pathogenicity<a class="elsevierStyleCrossRef" href="#bib0530">51</a>. Hence, our efforts will be devoted to increasing both the spectrum of genes of H. pylori (including variations in their structure) as well as on the host in a greater number of individuals. This could be useful to identify patients at risk of developing more aggressive alterations in the gastric mucosa who will require appropriate eradication treatments and a more rigorous follow-up to prevent progression to gastric cancer.FundingThis work was supported by a grant from the Universidad Nacional del Litoral, Santa Fe (Argentina) (CAI+D 2020 N° 50520190100198LI).Conflict of interestThe authors declare that they have no conflicts of interest." "textoCompletoSecciones" => array:1 [ "secciones" => array:13 [ 0 => array:3 [ "identificador" => "xres1862383" "titulo" => "Highlights" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0005" ] ] ] 1 => array:3 [ "identificador" => "xres1862384" "titulo" => "Abstract" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0010" ] ] ] 2 => array:2 [ "identificador" => "xpalclavsec1618574" "titulo" => "Keywords" ] 3 => array:3 [ "identificador" => "xres1862385" "titulo" => "Resumen" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0015" ] ] ] 4 => array:2 [ "identificador" => "xpalclavsec1618575" "titulo" => "Palabras clave" ] 5 => array:2 [ "identificador" => "sec0005" "titulo" => "Introduction" ] 6 => array:2 [ "identificador" => "sec0010" "titulo" => "Material and methods" ] 7 => array:2 [ "identificador" => "sec0015" "titulo" => "Results" ] 8 => array:2 [ "identificador" => "sec0020" "titulo" => "Discussion" ] 9 => array:2 [ "identificador" => "sec0025" "titulo" => "Funding" ] 10 => array:2 [ "identificador" => "sec0030" "titulo" => "Conflict of interest" ] 11 => array:2 [ "identificador" => "xack656309" "titulo" => "Acknowledgments" ] 12 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2021-08-15" "fechaAceptado" => "2022-04-07" "PalabrasClave" => array:2 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec1618574" "palabras" => array:5 [ 0 => "Helicobacter pylori" 1 => "Virulence factors" 2 => "IL-6" 3 => "Polymorphisms" 4 => "Intestinal metaplasia" ] ] ] "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec1618575" "palabras" => array:5 [ 0 => "Helicobacter pylori" 1 => "Factores de virulencia" 2 => "IL-6" 3 => "Polimorfismos" 4 => "Metaplasia intestinal" ] ] ] ] "tieneResumen" => true "highlights" => array:2 [ "titulo" => "Highlights" "resumen" => "<ul class="elsevierStyleList" id="lis0005"><li class="elsevierStyleListItem" id="lsti0005">•H. pylori genotypes and SNP-174G>C IL-6 in patients with gastritis were evaluated.</li><li class="elsevierStyleListItem" id="lsti0010">•More virulent genotypes and -174G/G IL-6 were found in active chronic gastritis IM+.</li><li class="elsevierStyleListItem" id="lsti0015">•Our results can be useful to identify patients at greater risk for adenocarcinoma.</li></ul>" ] "resumen" => array:2 [ "en" => array:2 [ "titulo" => "Abstract" "resumen" => "In Argentina, despite the important studies conducted on the prevalence of infection and the antibiotic resistance of Helicobacter pylori, there are no reports simultaneously analyzing a profile of virulence factors of the bacterium and polymorphisms in cytokine genes in patients with different alterations in the gastric mucosa (including intestinal metaplasia, IM). Our aim was to evaluate H. pylori genotypes in 132 adult patients with chronic gastritis presenting three different histological findings (inactive chronic gastritis, active chronic gastritis IM− and active chronic gastritis IM+) along with SNP-174 G>C in the IL-6 gene. cagA, vacA and babA2 genes were analyzed by multiplex PCR. The -174 G>C SNP IL-6 gene was analyzed by PCR-RFLP. Patients with active chronic gastritis IM+ showed the highest proportion of the cagA(+)/IL-6GG, cagA(+)/vacAm1s1/IL-6GG and cagA(+)/vacAm1s1/babA2(+)/IL-6GG combinations (p<0.05). There was 4-5 times greater probability of finding patients presenting the GG genotype for SNP-174 G>C IL-6, which in turn were infected with the most virulent H. pylori genotypes -cagA(+), cagA(+)/vacAm1s1 and cagA(+)/vacAm1s1/babA2- in the ACGIM+ group in comparison to the ICG group. Our results provide regional data to the idea that the transition towards severe alterations in the gastric mucosa would be the result of a balance between specific factors of H. pylori and inherent host factors. This fact can be useful to identify patients at greater risk and to select those individuals requiring appropriate eradication treatment to prevent progression to gastric cancer." ] "es" => array:2 [ "titulo" => "Resumen" "resumen" => "En Argentina, a pesar de los importantes estudios realizados sobre la prevalencia de infección y la resistencia a antibióticos de Helicobacter pylori, no existen reportes que analicen simultáneamente un perfil de factores de virulencia de la bacteria y polimorfismos en genes de citoquinas en pacientes con diferentes alteraciones en la mucosa gástrica (incluida la metaplasia intestinal [MI]). Nuestro objetivo fue evaluar genotipos de H. pylori en 132 pacientes adultos con gastritis crónica, con tres diferentes hallazgos histológicos (gastritis crónica inactiva [GCI], gastritis crónica activa [MI−] y gastritis crónica activa [MI+]), junto con el SNP-174 G>C en el gen de IL- 6. Los genes cagA, vacA y babA2 se analizaron mediante PCR multiplex. El SNP-174 G>C IL-6 se analizó mediante PCR-RFLP. Los pacientes con gastritis crónica activa MI+ mostraron la mayor proporción de combinaciones cagA(+)/IL-6GG, cagA(+)/vacAm1s1/IL-6GG y cagA(+)/vacAm1s1/babA2(+)/IL-6GG (p<0,05). Hubo 4-5 veces mayor probabilidad de encontrar pacientes con el genotipo GG en SNP-174 G>C IL-6 y a su vez infectados con los genotipos más virulentos de H. pylori—cagA(+), cagA(+)/vacAm1s1 y cagA(+)/vacAm1s1/babA2—en el grupo gastritis crónica activa MI+ en comparación con el grupo GCI. Nuestros resultados aportan datos regionales a la idea de que la transición hacia alteraciones más graves en la mucosa gástrica resultaría de un equilibrio entre factores específicos de H. pylori y factores inherentes al huésped. Esto puede ser útil para identificar pacientes con mayor riesgo y seleccionar aquellos individuos que requieran un apropiado tratamiento de erradicación para prevenir la progresión al cáncer gástrico." ] ] "multimedia" => array:3 [ 0 => array:7 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1270 "Ancho" => 1673 "Tamanyo" => 114120 ] ] "descripcion" => array:1 [ "en" => "Frequency of H. pylori genotypes in patients with chronic gastritis presenting different histological findings. (1) cagA(+); (2) vacAs1m1; (3) vacAs1m2; (4) vacAs2m1; (5) vacAs2m2; (6) babA2; (7) cagA(+)/vacAS1M1; (8) cagA(+)/vacAS1M1/babA2(+)." ] ] 1 => array:8 [ "identificador" => "tbl0005" "etiqueta" => "Table 1" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at1" "detalle" => "Table " "rol" => "short" ] ] "tabla" => array:2 [ "leyenda" => "ICG, inactive chronic gastritis; ACGIM−, active chronic gastritis without intestinal metaplasia; ACGIM+, active chronic gastritis with intestinal metaplasia. (*)(**) Significant differences (p<0.05)." "tablatextoimagen" => array:1 [ 0 => array:1 [ "tabla" => array:1 [ 0 => """ <table border="0" frame="\n \t\t\t\t\tvoid\n \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black"> \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">ICG (n=43) \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">ACGIM− (n=69) \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">ACGIM+ (n=20) \t\t\t\t\t\t\n \t\t\t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">SNP IL-6 GG \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t">27 (62.8%)(*) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t">49 (71%) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t">17 (85%)(*) \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">SNP IL-6 GC \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t">14 (32.6%) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t">18 (26.1%) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t">3 (15%) \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">SNP IL-6 CC \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t">2 (4.6%) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t">2 (2.9%) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t">0 (0%) \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">SNP IL-6 Alelo G \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t">68 (79%)(*) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t">116 (84%) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t">37 (92.5%)(*) \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">SNP IL-6 Alelo C \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t">18 (21%) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t">22 (16%) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t">3 (7.5%) \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">cagA(+)/IL-6 GG \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t">7 (16%)(*) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t">16 (23%)(**) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t">9 (45%)(*)(**) \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">cagA(+)/vacAS1M1/IL-6 GG \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t">7 (16%)(*) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t">16 (23%)(**) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t">9 (45%)(*)(**) \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">cagA(+)/vacAS1M1/babA2(+)/GG \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t">3 (7%)(*) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t">9 (13%)(**) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t">6 (30%)(*)(**) \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] ] ] ] "descripcion" => array:1 [ "en" => "Distribution of genotypes/alleles of IL-6 rs1800795 polimorphism and combinations of H. pylori virulence factors/GG IL-6 rs1800795 genotype in patients with different types of chronic gastritis." ] ] 2 => array:8 [ "identificador" => "tbl0010" "etiqueta" => "Table 2" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at2" "detalle" => "Table " "rol" => "short" ] ] "tabla" => array:2 [ "leyenda" => "ICG, inactive chronic gastritis; ACGIM−, active chronic gastritis without intestinal metaplasia; ACGIM+, active chronic gastritis with intestinal metaplasia. OR: Odds ratio. CI: confidence interval, ICG group was taken into account as a reference. p-values in boldface type indicate statistical significance." "tablatextoimagen" => array:1 [ 0 => array:1 [ "tabla" => array:1 [ 0 => """ <table border="0" frame="\n \t\t\t\t\tvoid\n \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black"> \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Group \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">OR \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">CI 95% \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">p \t\t\t\t\t\t\n \t\t\t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">ICG \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">1 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">N.D. \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">N.D. \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">cagA(+)/GG \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">ACGIM− \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">1.55 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">0.58 to 4.15 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">0.3809 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">ACGIM+ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">4.21 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">1.27 to 13.92 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">0.0186 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">cagA(+)/vacAm1s1/GG \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">ICG \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">1 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">N.D. \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">N.D. \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">ACGIM− \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">1.55 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">0.58 to 4.15 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">0.3809 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">ACGIM+ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">4.21 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">1.27 to 13.92 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">0.0186 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">cagA(+)/vacAm1s1/babA2(+)/GG \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">ICG \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">1 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">N.D. \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">N.D. \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">ACGIM− \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">2.00 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">0.51 to 7.84 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">0.3201 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">ACGIM+ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">5.71 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">1.25 to 25.96 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">0.0240 \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] ] ] ] "descripcion" => array:1 [ "en" => "Association of combinations of H. pylori virulence factors and GG IL-6 rs1800795 genotype in patients with different types of chronic gastritis." ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0015" "bibliografiaReferencia" => array:55 [ 0 => array:3 [ "identificador" => "bib0280" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Helicobacter pylori heterogeneity in patients with gastritis and peptic ulcer disease" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:7 [ 0 => "R.I. 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Helicobacter pylori: un balance entre bacterias y huésped

Pamela Buccia, Yanina Barbagliab, Fabián Tedeschia, Fabián Zalazara,

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fzalazar@fbcb.unl.edu.ar

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a Laboratorio de Práctica Profesional de Bioquímica, Facultad de Bioquímica y Ciencias Biológicas, Universidad Nacional del Litoral, Subsuelo Hospital “Dr. José María Cullen”, Avda. Freyre 2150, (S3000EOZ) Santa Fe, Argentina

b Servicio de Gastroenterologia, Subsuelo Hospital “Dr. José María Cullen”, Avda. Freyre 2150 (S3000EOZ) Santa Fe, Argentina

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    "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Introduction</span><p id="par0020" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Helicobacter pylori</span> &#40;<span class="elsevierStyleItalic">H&#46; pylori</span>&#41; is a gastric pathogen widely recognized as a causative agent of gastritis worldwide&#46; Furthermore&#44; <span class="elsevierStyleItalic">H&#46; pylori</span> is an important etiological agent for a multi-step cascade which&#44; starting from chronic gastritis&#44; can evolve to pre-neoplastic lesions &#40;such as intestinal metaplasia&#41;&#44; dysplasia and up to gastric adenocarcinoma<a class="elsevierStyleCrossRefs" href="#bib0325"><span class="elsevierStyleSup">10&#44;15&#44;17&#44;46&#44;52</span></a>&#46; In fact&#44; in 1994 it has been classified as a Class I carcinogen by the International Agency for Research on Cancer<a class="elsevierStyleCrossRef" href="#bib0365"><span class="elsevierStyleSup">18</span></a>&#46; In addition&#44; gastric cancer remains the 3rd leading cause of cancer-related death and the leading cause of infection-related cancer worldwide<a class="elsevierStyleCrossRef" href="#bib0335"><span class="elsevierStyleSup">12</span></a>&#46; Epidemiology of gastric cancer shows a high variability&#58; there are countries presenting high prevalence &#40;e&#46;g&#46;&#44; Korea&#44; Japan&#44; China&#44; Colombia&#44; Chile&#41; whereas others show low prevalence rates &#40;generally&#44; developed countries such as USA&#44; Canada and Australia&#41;&#46; Infection rates in Argentina are found at intermediate values&#44; with the highest values as well as the highest mortality rate from stomach cancer reported in the southern provinces<a class="elsevierStyleCrossRefs" href="#bib0330"><span class="elsevierStyleSup">11&#44;12&#44;25&#44;27&#44;37</span></a>&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">It has been mentioned that the cascade of events that would lead to adenocarcinoma seems to be triggered &#8211; among other causes &#8211; by bacterial-specific virulence factors &#40;such as the <span class="elsevierStyleItalic">cagA</span>&#44; <span class="elsevierStyleItalic">vacA</span>&#44; <span class="elsevierStyleItalic">babA2</span> gene&#41; as well as by factors such as polymorphisms in cytokine genes<a class="elsevierStyleCrossRefs" href="#bib0320"><span class="elsevierStyleSup">9&#44;21&#44;43&#44;50</span></a>&#46; In this sense&#44; greater mucosal Interleukin 6 &#40;IL-6&#41; levels in early gastric cancer with active <span class="elsevierStyleItalic">H&#46; pylori</span> infection than those without <span class="elsevierStyleItalic">H&#46; pylori</span> infection49&#44; have been observed&#46; In addition&#44; individuals with the G allele at position -174 in the promoter sequence of IL-6 have been shown to produce higher levels of IL-6<a class="elsevierStyleCrossRef" href="#bib0340"><span class="elsevierStyleSup">13</span></a>&#46; More recently&#44; the importance of IL-6 mediated stromal&#8211;epithelial cell interaction in gastric tumorigenesis has been suggested<a class="elsevierStyleCrossRef" href="#bib0385"><span class="elsevierStyleSup">22</span></a>&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">The abovementioned Correa&#39;s cascade is often referred to follow a linear progression&#59; nevertheless&#44; most patients present little or no change over time&#46; On the contrary&#44; other patients exhibiting a dynamic process alternating regression and&#47;or progression of lesions in their gastric mucosa and even rapid progression bypassing some of the putative steps is not an infrequent finding&#46; It has been suggested that intestinal metaplasia &#40;IM&#41; is a &#8220;point of no return&#8221;&#44; at which eradication is less effective at causing regression and indeed does not change the risk of progression in certain patients&#58; once IM is established&#44; eradication of <span class="elsevierStyleItalic">H&#46; pylori</span> only partially achieves a successful reduction of the risk of progression to adenocarcinoma and the genetic damage to gastric stem cells becomes irreversible<a class="elsevierStyleCrossRef" href="#bib0390"><span class="elsevierStyleSup">23</span></a>&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">In Argentina&#44; despite the important studies carried out in relation to the prevalence of infection and resistance of <span class="elsevierStyleItalic">H&#46; pylori</span> to the different antibiotics used for its eradication<a class="elsevierStyleCrossRefs" href="#bib0295"><span class="elsevierStyleSup">4&#44;19&#44;20&#44;34&#44;35&#44;48&#44;53</span></a> there are no reports simultaneously analyzing a profile of virulence factors of the bacterium and polymorphisms in cytokine genes of the host in patients with chronic gastritis showing different histopathological findings in the gastric mucosa &#40;including pre-neoplastic lesions such as intestinal metaplasia&#41;&#46; Hence&#44; our aim was to begin an evaluation of <span class="elsevierStyleItalic">H&#46; pylori</span> genotypes in adult patients residing in the north-central region of the Province of Santa Fe &#40;Argentina&#41; with different degrees of chronic gastritis&#44; along with SNP-174 G&#62;C in the promoter sequence of the IL-6 gene&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Material and methods</span><p id="par0040" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Patients and samples</span>&#46; Adult dyspeptic patients &#40;n&#61;270&#41; attending the Gastroenterology Service of &#8220;Dr&#46; Jos&#233; Mar&#237;a Cullen&#8221; Hospital &#40;Santa Fe&#44; Argentina&#41; were enrolled in the study after informed consent was obtained&#46; All of them underwent upper gastrointestinal endoscopy&#46; The study was approved by the Research Ethics Advisory Committee of the Facultad de Bioqu&#237;mica y Ciencias Biol&#243;gicas &#40;Universidad Nacional del Litoral&#41; as well as by the Ethics Committee of the &#8220;Hospital Dr&#46; J&#46;M&#46; Cullen&#8221;&#46; Patients who had received antibiotic therapy and&#47;or PPIs in the last 15 days were excluded from the study&#46; Both biopsy sampling and histological analyses were carried out following the modified Sydney standardized protocol&#46; Activity of gastritis was defined by the presence of neutrophils in the gastric mucosa&#46; Two additional samples were taken from antrum and corpus for the rapid urease test and molecular detection of <span class="elsevierStyleItalic">H&#46; pylori&#46;</span></p><p id="par0045" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">DNA purification and H&#46; pylori molecular detection</span>&#46; DNA purification was carried out following a procedure using Proteinase K as previously described<a class="elsevierStyleCrossRef" href="#bib0295"><span class="elsevierStyleSup">4</span></a>&#46; DNA integrity was evaluated by agarose gel electrophoresis&#59; DNA yields and purity were assessed by absorbance analysis at 260&#47;280<span class="elsevierStyleHsp" style=""></span>nm&#46; Purified DNA was stored at &#8722;20<span class="elsevierStyleHsp" style=""></span>&#176;C until use&#46; <span class="elsevierStyleItalic">H&#46; pylori</span> was studied in gastric biopsies by nested PCR targeting the hsp60 gene&#44; using previously reported conditions<a class="elsevierStyleCrossRef" href="#bib0375"><span class="elsevierStyleSup">20</span></a>&#46;</p><p id="par0050" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">H&#46; pylori cagA&#44; vacA and babA2 gene analysis</span>&#46; <span class="elsevierStyleItalic">cagA</span>&#44; <span class="elsevierStyleItalic">vacA</span> and <span class="elsevierStyleItalic">babA2</span> genes were analyzed by multiplex PCR using sequence specific primers<a class="elsevierStyleCrossRef" href="#bib0295"><span class="elsevierStyleSup">4</span></a>&#46;</p><p id="par0055" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Analysis of -174 G&#62;C single nucleotide polymorphism &#40;SNP&#41; in the IL-6 gene</span>&#46; The SNP-174 G&#62;C &#40;rs1800795&#41; in the promoter sequence of the IL-6 gene was analyzed by PCR-RFLP according to Guzman-Guzman et al<a class="elsevierStyleCrossRef" href="#bib0355"><span class="elsevierStyleSup">16</span></a>&#46; As a control&#44; the same SNPs were also analyzed in a group of <span class="elsevierStyleItalic">H&#46; pylori</span> &#40;&#8722;&#41; patients&#46; In all cases&#44; the -174 G&#62;C IL-6 polymorphism was in Hardy&#8211;Weinberg equilibrium&#44; which was similar to that recently reported by Strauss et al&#46;<a class="elsevierStyleCrossRef" href="#bib0500"><span class="elsevierStyleSup">45</span></a>&#44; when evaluating the distribution of IL-6 genotypes in seronegative and seropositive Argentine individuals for Chagas disease</p><p id="par0060" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Agarose gel electrophoresis</span>&#46; PCR products were analyzed by electrophoresis in 2&#37; agarose gels &#40;D1 Agarose&#44; Biodynamics&#44; Argentina&#41;&#46; All in vitro amplification reactions included an internal control &#40;human beta-globin gene&#41;&#46; PCR-RFLP fragments were resolved in 3&#37; agarose gels &#40;LE Agarose&#44; Inbio Highway&#44; Argentina&#41;&#46; All gels were prepared in the presence of a fluorescent stain and photographed under UV light&#46;</p><p id="par0065" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Statistical analysis</span>&#46; The association between categorical variables was evaluated using the Chi-square test and <span class="elsevierStyleItalic">Odds</span> ratio&#46; A <span class="elsevierStyleItalic">p</span>-value &#60;0&#46;05 was considered statistically significant&#46; A Hardy&#8211;Weinberg equilibrium analysis was carried out to evaluate the -174 G&#62;C polymorphism in the IL-6 gene&#46;</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Results</span><p id="par0070" class="elsevierStylePara elsevierViewall">The analysis was performed on samples from 132 patients with a histological diagnosis of chronic gastritis and with positive results for <span class="elsevierStyleItalic">H&#46; pylori</span> by <span class="elsevierStyleItalic">in vitro</span> amplification of the <span class="elsevierStyleItalic">hsp60</span> gene plus histological analysis and&#47;or rapid urease test &#40;in other words&#44; if a positive result was obtained by 2 out of 3 tests&#41;&#46;</p><p id="par0075" class="elsevierStylePara elsevierViewall">The age range of patients was 18&#8211;65 years&#44; with a mean value of 41&#46;7 years &#40;median<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>41&#41;&#46; With regard to gender&#44; 68&#46;1&#37; &#40;90&#41; and 31&#46;8&#37; &#40;42&#41; were women and men&#44; respectively&#44; in a 2&#46;14&#58;1 ratio&#46;</p><p id="par0080" class="elsevierStylePara elsevierViewall">When analyzing the <span class="elsevierStyleItalic">H&#46; pylori</span> genotypes present&#44; the presence of the <span class="elsevierStyleItalic">cagA</span> gene was detected in 34&#37; of all patients with chronic gastritis&#44; while the <span class="elsevierStyleItalic">babaA2</span> gene was present in 53&#37; of the samples analyzed&#46;</p><p id="par0085" class="elsevierStylePara elsevierViewall">All patients presented the <span class="elsevierStyleItalic">vacA</span> gene in its different variants&#58; 67&#37; corresponded to the m1s1 variant&#44; followed by the m2s2 and m2s1 variants&#44; in 25&#37; and 8&#37;&#44; respectively&#59; the presence of the <span class="elsevierStyleItalic">vacA</span>S2M1 variant was not detected&#46; The <span class="elsevierStyleItalic">cagA</span>&#40;&#43;&#41;&#47;<span class="elsevierStyleItalic">vacA</span> m1s1 combination &#40;reported as one of the most virulent&#41; was found in 32&#37; of the patients&#44; while the genotype called &#8220;triple virulent&#8221; <span class="elsevierStyleItalic">cagA</span>&#40;&#43;&#41;&#47;<span class="elsevierStyleItalic">vac</span>Am1s1&#47;<span class="elsevierStyleItalic">babA2</span> &#40;&#43;&#41; was present in 18&#37; of patients&#46;</p><p id="par0090" class="elsevierStylePara elsevierViewall">Taking into account the alterations in the gastric mucosa&#44; the total number of patients was reclassified into 3 groups &#40;a&#41; patients with inactive chronic gastritis &#40;ICG&#44; n<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>43&#59; age&#58; mean&#44; 41&#46;4&#59; range&#61;18&#8211;65&#41;&#44; &#40;b&#41; patients with active chronic gastritis without intestinal metaplasia &#40;ACGIM&#8722;&#44; n<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>69&#59; age&#58; mean&#44; 40&#46;3&#59; range<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>22&#8211;60&#41; and &#40;c&#41; patients with active chronic gastritis with intestinal metaplasia &#40;ACGIMI&#43;&#44; n<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>20&#59; age&#58; mean&#44; 46&#46;3&#59; range<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>28&#8211;64&#41;&#46; No significant differences were found in relation to the age of the different groups &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#62;<span class="elsevierStyleHsp" style=""></span>0&#46;05&#41;&#46;</p><p id="par0095" class="elsevierStylePara elsevierViewall">When analyzing the distribution of <span class="elsevierStyleItalic">H&#46; pylori</span> genotypes in the 3 above-mentioned groups&#44; although there were no significant differences between them&#44; interestingly the group of ACGIM&#43; patients exhibited the highest proportion of genotypes <span class="elsevierStyleItalic">cagA</span>&#40;&#43;&#41;&#44; <span class="elsevierStyleItalic">vacA</span>s1m1 and the combination <span class="elsevierStyleItalic">cagA</span>&#40;&#43;&#41;&#47;<span class="elsevierStyleItalic">vacA</span>m1s1 as well as the highest proportion of the &#8220;triple virulent&#8221; genotype <span class="elsevierStyleItalic">cagA</span>&#40;&#43;&#41;&#47;<span class="elsevierStyleItalic">vacA</span>m1s1&#47;<span class="elsevierStyleItalic">babA2</span>&#46;</p><p id="par0100" class="elsevierStylePara elsevierViewall">On the contrary&#44; although the ICG group showed the highest frequency of <span class="elsevierStyleItalic">babA2</span> &#40;&#43;&#41; strains&#44; it also had the lowest frequency of <span class="elsevierStyleItalic">cagA</span>&#40;&#43;&#41;&#44; <span class="elsevierStyleItalic">vacA</span>s1m1 genotypes and the <span class="elsevierStyleItalic">cagA</span>&#40;&#43;&#41;&#47;<span class="elsevierStyleItalic">vacA</span>m1s1 and <span class="elsevierStyleItalic">cagA</span>&#40;&#43;&#41; combinations&#47;<span class="elsevierStyleItalic">vacA</span>m1s1&#47;<span class="elsevierStyleItalic">babA2</span> &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0105" class="elsevierStylePara elsevierViewall">Then&#44; the -174 G&#62;C polymorphism in the promoter sequence of the IL-6 gene was analyzed in each group&#46; Based on our results&#44; the ACGIM&#43; group showed the highest proportion of both the high-expression GG haplotype and the G allele&#44; with significant differences compared to the ICG group &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#46;05&#41;&#46;</p><p id="par0110" class="elsevierStylePara elsevierViewall">Finally&#44; the -174 G&#62;C polymorphism in the IL-6 gene was analyzed in conjunction with the <span class="elsevierStyleItalic">H&#46; pylori</span> genotypes present in each group&#46; In this case&#44; in the group of patients with ACGIM&#43; we found the highest proportion of <span class="elsevierStyleItalic">cagA</span>&#40;&#43;&#41;&#47;IL-6 GG&#44; <span class="elsevierStyleItalic">cagA</span>&#40;&#43;&#41;&#47;<span class="elsevierStyleItalic">vacA</span>m1s1&#47;IL-6GG and <span class="elsevierStyleItalic">cagA</span>&#40;&#43;&#41;&#47;<span class="elsevierStyleItalic">vacA</span>m1s1&#47;<span class="elsevierStyleItalic">babA2</span> &#40;&#43;&#41;&#47;IL-6GG combinations&#44; with significant differences both with the ICG group and with the patients with ACGIM&#8722; &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#46;05&#41; &#40;<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>&#41;&#46;</p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia><p id="par0115" class="elsevierStylePara elsevierViewall">Furthermore&#44; there was 4&#8211;5 times greater probability of finding patients exhibiting the GG genotype for SNP -174 G&#62;C IL-6&#44; which in turn were infected with the most virulent <span class="elsevierStyleItalic">H&#46; pylori</span> genotypes &#8211; <span class="elsevierStyleItalic">cagA</span>&#40;&#43;&#41;&#44;<span class="elsevierStyleItalic">cagA</span>&#40;&#43;&#41;&#47;<span class="elsevierStyleItalic">vacA</span>m1s1 and <span class="elsevierStyleItalic">cagA</span>&#40;&#43;&#41;&#47;<span class="elsevierStyleItalic">vacA</span>m1s1&#47;<span class="elsevierStyleItalic">babA2</span> &#8211; in the ACGIM&#43; group in comparison to the patients of the ICG group &#40;<a class="elsevierStyleCrossRef" href="#tbl0010">Table 2</a>&#41;&#46;</p><elsevierMultimedia ident="tbl0010"></elsevierMultimedia></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Discussion</span><p id="par0120" class="elsevierStylePara elsevierViewall">The association between <span class="elsevierStyleItalic">H&#46; pylori</span> infection and gastric cancer is a well-known clinical event&#46; Moreover&#44; <span class="elsevierStyleItalic">H&#46; pylori</span> is recognized as one of the factors that would contribute to the development of the cascade of events described by Correa<a class="elsevierStyleCrossRef" href="#bib0325"><span class="elsevierStyleSup">10</span></a>&#44; which begins with chronic gastritis followed by the development of pre-neoplastic lesions &#40;such as intestinal metaplasia&#41; leading to adenocarcinoma<a class="elsevierStyleCrossRef" href="#bib0435"><span class="elsevierStyleSup">32</span></a>&#46; On the other hand&#44; different articles have shown important differences in relation to the infecting <span class="elsevierStyleItalic">H&#46; pylori</span> genotypes as well as the epidemiology of gastric cancer around the world and even within the same country<a class="elsevierStyleCrossRefs" href="#bib0300"><span class="elsevierStyleSup">5&#44;8&#44;38&#44;47&#44;55</span></a>&#46; Furthermore&#44; different studies have explored the role of polymorphisms in interleukins associated with pre-neoplastic lesions in patients infected with <span class="elsevierStyleItalic">H&#46;</span><span class="elsevierStyleItalic">pylori</span><a class="elsevierStyleCrossRefs" href="#bib0485"><span class="elsevierStyleSup">42&#44;54</span></a>&#46;</p><p id="par0125" class="elsevierStylePara elsevierViewall">In this context&#44; our country has a vast surface area and although important studies in relation to the prevalence of infection as well as resistance to antibiotics have been published<a class="elsevierStyleCrossRefs" href="#bib0295"><span class="elsevierStyleSup">4&#44;19&#44;20&#44;34&#44;35&#44;48&#44;53</span></a>&#44; to our knowledge there are no studies that simultaneously analyze&#58; &#40;a&#41; the profile of virulence factors of the bacterium&#44; &#40;b&#41; the polymorphisms in the cytokine genes of patients with chronic gastritis and &#40;c&#41; the histopathological findings in the gastric mucosa&#44; including pre-neoplastic lesions such as intestinal metaplasia&#46; Taking this into account&#44; our aim was to begin a study focused on these variables in adult patients with chronic gastritis from the north-central region of Santa Fe province &#40;Argentina&#41;&#46;</p><p id="par0130" class="elsevierStylePara elsevierViewall">Based on our results&#44; the frequency of the best-studied virulence factors &#40;<span class="elsevierStyleItalic">cagA</span>&#44; <span class="elsevierStyleItalic">vacA</span> and <span class="elsevierStyleItalic">babA2</span>&#41; in patients with chronic gastritis is related to previous studies in Argentina<a class="elsevierStyleCrossRefs" href="#bib0305"><span class="elsevierStyleSup">6&#44;24&#44;26&#44;28&#44;31&#44;48</span></a>&#46; However&#44; some differences can be highlighted&#58; the frequency of the <span class="elsevierStyleItalic">cagA</span> gene found in our study &#40;34&#37;&#41; is similar to that reported in the western region &#40;30&#8211;40&#46;8&#37;&#41;<a class="elsevierStyleCrossRefs" href="#bib0415"><span class="elsevierStyleSup">28&#44;48</span></a>&#59; however&#44; lower than the data for Buenos Aires city &#40;71&#8211;84&#37;&#41;<a class="elsevierStyleCrossRefs" href="#bib0305"><span class="elsevierStyleSup">6&#44;24&#44;26</span></a>&#46; On the other hand&#44; as reported by other authors in our country&#44; the <span class="elsevierStyleItalic">vacA</span>m1s1 variant was predominant in the group of patients with chronic gastritis studied<a class="elsevierStyleCrossRefs" href="#bib0305"><span class="elsevierStyleSup">6&#44;24&#44;28&#44;48</span></a>&#46; With respect to the virulence factor <span class="elsevierStyleItalic">bab</span>A2&#44; we found a considerably higher proportion of patients carrying this gene than that reported by Medina et al&#46;<a class="elsevierStyleCrossRef" href="#bib0430"><span class="elsevierStyleSup">31</span></a>&#44; who found 9&#46;7&#37; in gastric biopsies of patients from another geographical region of our country&#46; This could represent a real difference in the circulating genotypes or might be due to different experimental conditions&#44; fundamentally given by the sequence of primers used for the amplification of the <span class="elsevierStyleItalic">babA2</span> gene&#44; as recently indicated<a class="elsevierStyleCrossRef" href="#bib0495"><span class="elsevierStyleSup">44</span></a>&#44; as well as by the presence of allelic variations in the <span class="elsevierStyleItalic">bab</span>A2 gene owing to microevolution phenomena described during colonization in some patients<a class="elsevierStyleCrossRef" href="#bib0420"><span class="elsevierStyleSup">29</span></a>&#46; This microheterogeneity has been reported previously in interesting studies by Matteo et al&#46;<a class="elsevierStyleCrossRef" href="#bib0425"><span class="elsevierStyleSup">30</span></a> and Armitano et al&#46;<a class="elsevierStyleCrossRef" href="#bib0280"><span class="elsevierStyleSup">1</span></a> where the <span class="elsevierStyleItalic">cag</span> pathogenicity island &#40;<span class="elsevierStyleItalic">cag</span>PAI&#41;&#44; <span class="elsevierStyleItalic">vacA</span>&#44; <span class="elsevierStyleItalic">bab</span>&#44; <span class="elsevierStyleItalic">oipA</span>&#44; <span class="elsevierStyleItalic">dupA</span> status and the presence of several genes from the genomic plasticity zone were studied to analyze intra-host variation in patients with chronic gastritis and peptic ulcer disease&#46; In these studies&#44; an inter-niche variability was proven for most of the genes analyzed in the <span class="elsevierStyleItalic">cag</span>PAI&#44; for the genes <span class="elsevierStyleItalic">oipA</span>&#44; <span class="elsevierStyleItalic">dupA</span> and for those in the plasticity region and&#44; in a lesser extent&#44; for the <span class="elsevierStyleItalic">bab</span> gene&#46; However&#44; such significant variability was not observed for the <span class="elsevierStyleItalic">cagA</span> and <span class="elsevierStyleItalic">vacA</span> genes&#46; Matteo et al&#46;<a class="elsevierStyleCrossRef" href="#bib0425"><span class="elsevierStyleSup">30</span></a> found that 37&#47;40 patients had isolates with the same profile for the <span class="elsevierStyleItalic">vacA</span> gene whereas Armitano et al&#46;<a class="elsevierStyleCrossRef" href="#bib0280"><span class="elsevierStyleSup">1</span></a>&#44; identified that 24&#47;28 and 25&#47;28 patients had <span class="elsevierStyleItalic">H&#46; pylori</span> isolates with the same status for the <span class="elsevierStyleItalic">cagA</span> and <span class="elsevierStyleItalic">vacA</span> genes respectively&#44; in the different niches studied&#46;</p><p id="par0135" class="elsevierStylePara elsevierViewall">In the next analysis&#44; when classifying the patients into groups according to the histological findings &#40;inactive chronic gastritis&#44; active chronic gastritis IM&#8722; and active chronic gastritis IM&#43;&#41;&#44; as expected&#44; we observed a trend towards a higher proportion of patients carrying the most virulent genotypes in patients with active chronic gastritis IM&#43;&#44; although differences were not statistically significant&#46; However&#44; when the analysis of the -174 G&#62;C SNP in the IL-6 gene was included&#44; we found a higher proportion of the IL-6 GG genotype in patients infected with both <span class="elsevierStyleItalic">cagA</span>&#40;&#43;&#41; <span class="elsevierStyleItalic">H&#46; pylori</span> strains as well as with the combinations <span class="elsevierStyleItalic">cagA</span>&#40;&#43;&#41;&#47;<span class="elsevierStyleItalic">vacA</span>s1m1 and <span class="elsevierStyleItalic">cagA</span>&#43;&#47;<span class="elsevierStyleItalic">vacA</span>s1m1&#47;<span class="elsevierStyleItalic">babA2</span> &#40;&#43;&#41; in the active chronic gastritis IM&#43; group in relation to the other two groups&#46; In this case&#44; differences were significant in patients with inactive chronic gastritis as well as in patients with active chronic gastritis that did not exhibit intestinal metaplasia&#46;</p><p id="par0140" class="elsevierStylePara elsevierViewall">Previous studies were conducted to analyze the impact of polymorphisms at position -174 of the IL-6 promoter in the development of gastric pathologies in the presence of <span class="elsevierStyleItalic">H&#46; pylori</span>&#44; with contradictory results&#46; Similarly to our study&#44; Gatti et al&#46;<a class="elsevierStyleCrossRef" href="#bib0345"><span class="elsevierStyleSup">14</span></a> found an association between the GG alleles of IL-6 &#40;-174 base&#41; and the presence of gastric adenocarcinoma&#44; independently of the tumor type &#40;diffuse or intestinal&#41;&#46; Similarly&#44; a study conducted in Portugal reported a higher frequency of the IL-6 -174C&#47;G genotype in the gastric cancer cases analyzed<a class="elsevierStyleCrossRef" href="#bib0475"><span class="elsevierStyleSup">40</span></a>&#46; Attar et al&#46;<a class="elsevierStyleCrossRef" href="#bib0285"><span class="elsevierStyleSup">2</span></a> also found a high frequency of the G allele and the GG genotype in patients compared to control subjects&#44; suggesting that the polymorphism could influence the susceptibility to gastric cancer&#46; On the other hand&#44; although our findings differ from those by Ramis et al&#46;<a class="elsevierStyleCrossRef" href="#bib0455"><span class="elsevierStyleSup">36</span></a> and Santos et al&#46;<a class="elsevierStyleCrossRef" href="#bib0480"><span class="elsevierStyleSup">41</span></a> who found no correlation between polymorphisms in IL-6 and a higher risk of gastric carcinoma&#44; they are consistent with the possibility of finding greater lesions in the gastric mucosa of those patients infected with more virulent strains of <span class="elsevierStyleItalic">H&#46; pylori</span> with a potential higher local inflammatory response triggered by a greater expression of pro-inflammatory cytokines such as IL-6&#46; In this sense&#44; individuals with the G allele at position -174 have been shown to produce higher levels of IL-6<a class="elsevierStyleCrossRef" href="#bib0340"><span class="elsevierStyleSup">13</span></a>&#46; Furthermore&#44; mucosal IL-6 levels were also greater in early gastric cancer with active <span class="elsevierStyleItalic">H&#46; pylori</span> infection than without <span class="elsevierStyleItalic">H&#46; pylori</span> infection&#44; and the levels decreased dramatically after the eradication of infection<a class="elsevierStyleCrossRef" href="#bib0520"><span class="elsevierStyleSup">49</span></a>&#46; In a similar way&#44; a positive correlation between mucosal IL-6 mRNA expression level and virulence factors of <span class="elsevierStyleItalic">H&#46; pylori</span> in Iranian adult patients with chronic gastritis has been recently reported<a class="elsevierStyleCrossRef" href="#bib0290"><span class="elsevierStyleSup">3</span></a>&#46; In addition&#44; Kinoshita et al&#46;<a class="elsevierStyleCrossRef" href="#bib0385"><span class="elsevierStyleSup">22</span></a>&#44; among other authors&#44; suggested the importance of IL-6 mediated stromal&#8211;epithelial cell interaction in gastric tumorigenesis&#46;</p><p id="par0145" class="elsevierStylePara elsevierViewall">Due to the fact that Latin America is a region with one of the highest mortality rates due to gastric cancer in the world<a class="elsevierStyleCrossRef" href="#bib0310"><span class="elsevierStyleSup">7</span></a> and since it has been mentioned that&#44; in some individuals&#44; intestinal metaplasia might be a &#8220;point of no return&#8221; to the development of gastric adenocarcinoma&#44; we consider relevant to report the first analysis in our region &#40;Santa Fe&#44; Argentina&#41; of <span class="elsevierStyleItalic">H&#46; pylori</span> genotypes and IL-6 SNP in patients with different types of gastritis&#44; including pre-neoplastic lesions such as intestinal metaplasia&#46; It should be noted that our analysis not only included the presence&#47;absence of <span class="elsevierStyleItalic">H&#46; pylori</span> associated to gastritis and pre-neoplastic alterations but also the identification of <span class="elsevierStyleItalic">H&#46; pylori</span> genotypes along with the -174 G&#62;C polymorphism on the IL-6 gene in each patient&#46;</p><p id="par0150" class="elsevierStylePara elsevierViewall">These results obtained so far for our region would be in accordance with the idea that the transition towards more severe alterations during <span class="elsevierStyleItalic">H&#46; pylori</span> infection would result from a balance between specific factors of the bacterium and host factors that modulate the inflammatory response during infection of the gastric mucosa&#46;</p><p id="par0155" class="elsevierStylePara elsevierViewall">In this sense&#44; a recent review by Rudnicka et al&#46;<a class="elsevierStyleCrossRef" href="#bib0470"><span class="elsevierStyleSup">39</span></a> analyzed results from large-scale epidemiological studies&#44; literature meta-analyses as well as from clinical and animal model studies focusing on the search of host immune system regulators &#40;such SNPs in cytokines&#47;growth factors&#41; together with <span class="elsevierStyleItalic">H&#46; pylori</span> virulence factors that facilitate the development of pre-cancerous and cancerous lesions&#44; in the context of environmental and geographical determinants&#46; Among the bacterial determinants related to gastric cancer development&#44; they highlighted the infection with <span class="elsevierStyleItalic">cagA</span>-positive &#40;particularly with a high number of EPIYA-C phosphorylation motifs&#41; and <span class="elsevierStyleItalic">vac</span>A-positive isolates &#40;in particular s1&#47;m1 allele strains&#41;&#46; They also reported that the combined genotyping of bacterial and host determinants suggests that the accumulation of polymorphisms favoring host and bacterial features increases the risk for precancerous and cancerous lesions in patients and they also suggested that biological determinants are urgently needed to predict the clinical course of infection in individuals with confirmed <span class="elsevierStyleItalic">H&#46; pylori</span> infection&#46;</p><p id="par0160" class="elsevierStylePara elsevierViewall">Furthermore&#44; a whole-genome analysis was recently used to study 723 <span class="elsevierStyleItalic">H&#46; pylori</span> genomes from different regions of the world in order to compare American &#40;from 14 geographical sites across America&#44; from Canada to Argentina&#41; versus non-American populations<a class="elsevierStyleCrossRef" href="#bib0440"><span class="elsevierStyleSup">33</span></a>&#46; In this study&#44; genetic variants that were more common in the Americas than in the populations from other continents were identified&#44; mainly resulting in non-synonymous mutations in functionally relevant regions of virulence genes &#40;among them&#44; <span class="elsevierStyleItalic">cagA</span>&#44; <span class="elsevierStyleItalic">vacA</span> and <span class="elsevierStyleItalic">babA</span> genes&#41;&#44; in domains known to interact with molecules of the host&#46; Based on previous reports&#44; it was suggested that the progression to serious clinical diseases&#44; such as gastric cancer&#44; is associated with the carriage of specific genotypes of the bacterium&#44; in particular those that carry genes linked with virulence&#44; concluding that the differences found between American and non-American <span class="elsevierStyleItalic">H&#46; pylori</span> genomes could reflect a co-evolutionary process potentially contributing to the high risk of gastric cancer in the region&#46;</p><p id="par0165" class="elsevierStylePara elsevierViewall">To date&#44; our work has aimed at analyzing the presence or absence of the most studied genes in <span class="elsevierStyleItalic">H&#46; pylori</span> &#40;<span class="elsevierStyleItalic">cagA</span>&#44; <span class="elsevierStyleItalic">vacA</span> and <span class="elsevierStyleItalic">babA</span>2&#41; and their association with the severity of gastric lesions without considering variations in their structure &#40;such as those due to the presence of different types&#47;number of EPIYA sequences&#41;&#44; additional polymorphisms in the <span class="elsevierStyleItalic">cagA</span> gene or the integrity of <span class="elsevierStyleItalic">cag</span> PAI which mediates efficient CagA translocation&#44; important for the commencement of pathogenicity<a class="elsevierStyleCrossRef" href="#bib0530"><span class="elsevierStyleSup">51</span></a>&#46; Hence&#44; our efforts will be devoted to increasing both the spectrum of genes of <span class="elsevierStyleItalic">H&#46; pylori</span> &#40;including variations in their structure&#41; as well as on the host in a greater number of individuals&#46; This could be useful to identify patients at risk of developing more aggressive alterations in the gastric mucosa who will require appropriate eradication treatments and a more rigorous follow-up to prevent progression to gastric cancer&#46;</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Funding</span><p id="par0170" class="elsevierStylePara elsevierViewall">This work was supported by a grant from the <span class="elsevierStyleGrantSponsor" id="gs1">Universidad Nacional del Litoral</span>&#44; Santa Fe &#40;Argentina&#41; &#40;CAI&#43;D 2020 N&#176; 50520190100198LI&#41;&#46;</p></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Conflict of interest</span><p id="par0175" class="elsevierStylePara elsevierViewall">The authors declare that they have no conflicts of interest&#46;</p></span></span>"
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          "identificador" => "xres1862383"
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        1 => array:3 [
          "identificador" => "xres1862384"
          "titulo" => "Abstract"
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              "identificador" => "abst0010"
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        2 => array:2 [
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          "titulo" => "Keywords"
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          "titulo" => "Resumen"
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          "titulo" => "Palabras clave"
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          "titulo" => "Introduction"
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          "titulo" => "Material and methods"
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          "titulo" => "Results"
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          "titulo" => "Discussion"
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        9 => array:2 [
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          "titulo" => "Funding"
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          "titulo" => "Conflict of interest"
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        11 => array:2 [
          "identificador" => "xack656309"
          "titulo" => "Acknowledgments"
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        12 => array:1 [
          "titulo" => "References"
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    "pdfFichero" => "main.pdf"
    "tienePdf" => true
    "fechaRecibido" => "2021-08-15"
    "fechaAceptado" => "2022-04-07"
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            0 => "<span class="elsevierStyleItalic">Helicobacter pylori</span>"
            1 => "Virulence factors"
            2 => "IL-6"
            3 => "Polymorphisms"
            4 => "Intestinal metaplasia"
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            0 => "<span class="elsevierStyleItalic">Helicobacter pylori</span>"
            1 => "Factores de virulencia"
            2 => "IL-6"
            3 => "Polimorfismos"
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    "highlights" => array:2 [
      "titulo" => "Highlights"
      "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall"><ul class="elsevierStyleList" id="lis0005"><li class="elsevierStyleListItem" id="lsti0005"><span class="elsevierStyleLabel">&#8226;</span><p id="par0005" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">H&#46; pylori</span> genotypes and SNP-174G&#62;C IL-6 in patients with gastritis were evaluated&#46;</p></li><li class="elsevierStyleListItem" id="lsti0010"><span class="elsevierStyleLabel">&#8226;</span><p id="par0010" class="elsevierStylePara elsevierViewall">More virulent genotypes and -174G&#47;G IL-6 were found in active chronic gastritis IM&#43;&#46;</p></li><li class="elsevierStyleListItem" id="lsti0015"><span class="elsevierStyleLabel">&#8226;</span><p id="par0015" class="elsevierStylePara elsevierViewall">Our results can be useful to identify patients at greater risk for adenocarcinoma&#46;</p></li></ul></p></span>"
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        "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">In Argentina&#44; despite the important studies conducted on the prevalence of infection and the antibiotic resistance of <span class="elsevierStyleItalic">Helicobacter pylori</span>&#44; there are no reports simultaneously analyzing a profile of virulence factors of the bacterium and polymorphisms in cytokine genes in patients with different alterations in the gastric mucosa &#40;including intestinal metaplasia&#44; IM&#41;&#46; Our aim was to evaluate <span class="elsevierStyleItalic">H&#46; pylori</span> genotypes in 132 adult patients with chronic gastritis presenting three different histological findings &#40;inactive chronic gastritis&#44; active chronic gastritis IM&#8722; and active chronic gastritis IM&#43;&#41; along with SNP-174 G&#62;C in the IL-6 gene&#46; <span class="elsevierStyleItalic">cagA</span>&#44; <span class="elsevierStyleItalic">vacA</span> and <span class="elsevierStyleItalic">babA2</span> genes were analyzed by multiplex PCR&#46; The -174 G&#62;C SNP IL-6 gene was analyzed by PCR-RFLP&#46; Patients with active chronic gastritis IM&#43; showed the highest proportion of the <span class="elsevierStyleItalic">cagA</span>&#40;&#43;&#41;&#47;IL-6GG&#44; <span class="elsevierStyleItalic">cagA</span>&#40;&#43;&#41;&#47;<span class="elsevierStyleItalic">vacA</span>m1s1&#47;IL-6GG and <span class="elsevierStyleItalic">cagA</span>&#40;&#43;&#41;&#47;<span class="elsevierStyleItalic">vacA</span>m1s1&#47;<span class="elsevierStyleItalic">babA</span>2&#40;&#43;&#41;&#47;IL-6GG combinations &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#46;05&#41;&#46; There was 4-5 times greater probability of finding patients presenting the GG genotype for SNP-174 G&#62;C IL-6&#44; which in turn were infected with the most virulent <span class="elsevierStyleItalic">H&#46; pylori</span> genotypes -<span class="elsevierStyleItalic">cagA</span>&#40;&#43;&#41;&#44; <span class="elsevierStyleItalic">cagA</span>&#40;&#43;&#41;&#47;<span class="elsevierStyleItalic">vacA</span>m1s1 and <span class="elsevierStyleItalic">cagA</span>&#40;&#43;&#41;&#47;<span class="elsevierStyleItalic">vacA</span>m1s1&#47;<span class="elsevierStyleItalic">babA2</span>- in the ACGIM&#43; group in comparison to the ICG group&#46; Our results provide regional data to the idea that the transition towards severe alterations in the gastric mucosa would be the result of a balance between specific factors of <span class="elsevierStyleItalic">H&#46; pylori</span> and inherent host factors&#46; This fact can be useful to identify patients at greater risk and to select those individuals requiring appropriate eradication treatment to prevent progression to gastric cancer&#46;</p></span>"
      ]
      "es" => array:2 [
        "titulo" => "Resumen"
        "resumen" => "<span id="abst0015" class="elsevierStyleSection elsevierViewall"><p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">En Argentina&#44; a pesar de los importantes estudios realizados sobre la prevalencia de infecci&#243;n y la resistencia a antibi&#243;ticos de <span class="elsevierStyleItalic">Helicobacter pylori</span>&#44; no existen reportes que analicen simult&#225;neamente un perfil de factores de virulencia de la bacteria y polimorfismos en genes de citoquinas en pacientes con diferentes alteraciones en la mucosa g&#225;strica &#40;incluida la metaplasia intestinal &#91;MI&#93;&#41;&#46; Nuestro objetivo fue evaluar genotipos de <span class="elsevierStyleItalic">H&#46; pylori</span> en 132 pacientes adultos con gastritis cr&#243;nica&#44; con tres diferentes hallazgos histol&#243;gicos &#40;gastritis cr&#243;nica inactiva &#91;GCI&#93;&#44; gastritis cr&#243;nica activa &#91;MI&#8722;&#93; y gastritis cr&#243;nica activa &#91;MI&#43;<span class="elsevierStyleMonospace">&#93;</span>&#41;&#44; junto con el SNP-174 G&#62;C en el gen de IL- 6&#46; Los genes <span class="elsevierStyleItalic">cagA</span>&#44; <span class="elsevierStyleItalic">vacA</span> y <span class="elsevierStyleItalic">babA2</span> se analizaron mediante PCR multiplex&#46; El SNP-174 G&#62;C IL-6 se analiz&#243; mediante PCR-RFLP&#46; Los pacientes con gastritis cr&#243;nica activa MI&#43; mostraron la mayor proporci&#243;n de combinaciones <span class="elsevierStyleItalic">cagA</span>&#40;&#43;&#41;&#47;IL-6GG&#44; <span class="elsevierStyleItalic">cagA</span>&#40;&#43;&#41;&#47;<span class="elsevierStyleItalic">vacA</span>m1s1&#47;IL-6GG y <span class="elsevierStyleItalic">cagA</span>&#40;&#43;&#41;&#47;<span class="elsevierStyleItalic">vacA</span>m1s1&#47;<span class="elsevierStyleItalic">babA2</span>&#40;&#43;&#41;&#47;IL-6GG &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;05&#41;&#46; Hubo 4-5 veces mayor probabilidad de encontrar pacientes con el genotipo GG en SNP-174 G&#62;C IL-6 y a su vez infectados con los genotipos m&#225;s virulentos de <span class="elsevierStyleItalic">H&#46; pylori</span>&#8212;<span class="elsevierStyleItalic">cagA</span>&#40;&#43;&#41;&#44; <span class="elsevierStyleItalic">cagA</span>&#40;&#43;&#41;&#47;<span class="elsevierStyleItalic">vacA</span>m1s1 y <span class="elsevierStyleItalic">cagA</span>&#40;&#43;&#41;&#47;<span class="elsevierStyleItalic">vacA</span>m1s1&#47;<span class="elsevierStyleItalic">babA2</span>&#8212;en el grupo gastritis cr&#243;nica activa MI&#43; en comparaci&#243;n con el grupo GCI&#46; Nuestros resultados aportan datos regionales a la idea de que la transici&#243;n hacia alteraciones m&#225;s graves en la mucosa g&#225;strica resultar&#237;a de un equilibrio entre factores espec&#237;ficos de <span class="elsevierStyleItalic">H&#46; pylori</span> y factores inherentes al hu&#233;sped&#46; Esto puede ser &#250;til para identificar pacientes con mayor riesgo y seleccionar aquellos individuos que requieran un apropiado tratamiento de erradicaci&#243;n para prevenir la progresi&#243;n al c&#225;ncer g&#225;strico&#46;</p></span>"
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          "en" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Frequency of <span class="elsevierStyleItalic">H&#46; pylori</span> genotypes in patients with chronic gastritis presenting different histological findings&#46; &#40;1&#41; <span class="elsevierStyleItalic">cag</span>A&#40;&#43;&#41;&#59; &#40;2&#41; <span class="elsevierStyleItalic">vac</span>As1m1&#59; &#40;3&#41; <span class="elsevierStyleItalic">vac</span>As1m2&#59; &#40;4&#41; <span class="elsevierStyleItalic">vac</span>As2m1&#59; &#40;5&#41; <span class="elsevierStyleItalic">vac</span>As2m2&#59; &#40;6&#41; <span class="elsevierStyleItalic">bab</span>A2&#59; &#40;7&#41; <span class="elsevierStyleItalic">cag</span>A&#40;&#43;&#41;&#47;<span class="elsevierStyleItalic">vac</span>AS1M1&#59; &#40;8&#41; <span class="elsevierStyleItalic">cag</span>A&#40;&#43;&#41;&#47;<span class="elsevierStyleItalic">vac</span>AS1M1&#47;<span class="elsevierStyleItalic">bab</span>A2&#40;&#43;&#41;&#46;</p>"
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          "leyenda" => "<p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">ICG&#44; inactive chronic gastritis&#59; ACGIM&#8722;&#44; active chronic gastritis without intestinal metaplasia&#59; ACGIM&#43;&#44; active chronic gastritis with intestinal metaplasia&#46; &#40;&#42;&#41;&#40;&#42;&#42;&#41; Significant differences &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#46;05&#41;&#46;</p>"
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                  \t\t\t\t">SNP IL-6 GG&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">cag</span>A&#40;&#43;&#41;&#47;IL-6 GG&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">cag</span>A&#40;&#43;&#41;&#47;<span class="elsevierStyleItalic">vac</span>AS1M1&#47;<span class="elsevierStyleItalic">bab</span>A2&#40;&#43;&#41;&#47;GG&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t</td></tr></tbody></table>
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          "en" => "<p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">Distribution of genotypes&#47;alleles of IL-6 rs1800795 polimorphism and combinations of <span class="elsevierStyleItalic">H&#46; pylori</span> virulence factors&#47;GG IL-6 rs1800795 genotype in patients with different types of chronic gastritis&#46;</p>"
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          "leyenda" => "<p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">ICG&#44; inactive chronic gastritis&#59; ACGIM&#8722;&#44; active chronic gastritis without intestinal metaplasia&#59; ACGIM&#43;&#44; active chronic gastritis with intestinal metaplasia&#46; OR&#58; <span class="elsevierStyleItalic">Odds</span> ratio&#46; CI&#58; confidence interval&#44; ICG group was taken into account as a reference&#46; <span class="elsevierStyleItalic">p</span>-values in boldface type indicate statistical significance&#46;</p>"
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                  \t\t\t\t">0&#46;58 to 4&#46;15&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">cagA</span>&#40;&#43;&#41;&#47;<span class="elsevierStyleItalic">vacA</span>m1s1&#47;GG&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t  " align="left" valign="\n
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                  \t\t\t\t  " align="left" valign="\n
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                  \t\t\t\t">N&#46;D&#46;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="\n
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                  \t\t\t\t  " align="left" valign="\n
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                  \t\t\t\t">N&#46;D&#46;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t\ttable-entry\n
                  \t\t\t\t  " align="" valign="\n
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                  \t\t\t\t  " align="left" valign="\n
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                  \t\t\t\t">ACGIM&#8722;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="\n
                  \t\t\t\t\ttable-entry\n
                  \t\t\t\t  " align="left" valign="\n
                  \t\t\t\t\ttop\n
                  \t\t\t\t">1&#46;55&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="\n
                  \t\t\t\t\ttable-entry\n
                  \t\t\t\t  " align="left" valign="\n
                  \t\t\t\t\ttop\n
                  \t\t\t\t">0&#46;58 to 4&#46;15&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="\n
                  \t\t\t\t\ttable-entry\n
                  \t\t\t\t  " align="left" valign="\n
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                  \t\t\t\t">0&#46;3809&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n
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                  \t\t\t\t  " align="" valign="\n
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                  \t\t\t\t</td><td class="td" title="\n
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                  \t\t\t\t  " align="left" valign="\n
                  \t\t\t\t\ttop\n
                  \t\t\t\t">ACGIM&#43;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="\n
                  \t\t\t\t\ttable-entry\n
                  \t\t\t\t  " align="left" valign="\n
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                  \t\t\t\t  " align="left" valign="\n
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                  \t\t\t\t">1&#46;27 to 13&#46;92&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="\n
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                  \t\t\t\t">0&#46;0186&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n
                  \t\t\t\t\ttable-entry\n
                  \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">cagA</span>&#40;&#43;&#41;&#47;<span class="elsevierStyleItalic">vacA</span>m1s1&#47;<span class="elsevierStyleItalic">babA2</span>&#40;&#43;&#41;&#47;GG&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="\n
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                  \t\t\t\t  " align="left" valign="\n
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                  \t\t\t\t">ICG&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t  " align="left" valign="\n
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                  \t\t\t\t">N&#46;D&#46;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t  " align="left" valign="\n
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                  \t\t\t\t\ttable-entry\n
                  \t\t\t\t  " align="" valign="\n
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                  \t\t\t\t">&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="\n
                  \t\t\t\t\ttable-entry\n
                  \t\t\t\t  " align="left" valign="\n
                  \t\t\t\t\ttop\n
                  \t\t\t\t">ACGIM&#8722;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="\n
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                  \t\t\t\t  " align="left" valign="\n
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                  \t\t\t\t">2&#46;00&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="\n
                  \t\t\t\t\ttable-entry\n
                  \t\t\t\t  " align="left" valign="\n
                  \t\t\t\t\ttop\n
                  \t\t\t\t">0&#46;51 to 7&#46;84&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="\n
                  \t\t\t\t\ttable-entry\n
                  \t\t\t\t  " align="left" valign="\n
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                  \t\t\t\t">0&#46;3201&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n
                  \t\t\t\t\ttable-entry\n
                  \t\t\t\t  " align="" valign="\n
                  \t\t\t\t\ttop\n
                  \t\t\t\t">&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="\n
                  \t\t\t\t\ttable-entry\n
                  \t\t\t\t  " align="left" valign="\n
                  \t\t\t\t\ttop\n
                  \t\t\t\t">ACGIM&#43;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="\n
                  \t\t\t\t\ttable-entry\n
                  \t\t\t\t  " align="left" valign="\n
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                  \t\t\t\t">5&#46;71&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="\n
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                  \t\t\t\t  " align="left" valign="\n
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                  \t\t\t\t">1&#46;25 to 25&#46;96&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="\n
                  \t\t\t\t\ttable-entry\n
                  \t\t\t\t  " align="left" valign="\n
                  \t\t\t\t\ttop\n
                  \t\t\t\t"><span class="elsevierStyleBold">0&#46;0240</span>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr></tbody></table>
                  """
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        "descripcion" => array:1 [
          "en" => "<p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">Association of combinations of <span class="elsevierStyleItalic">H&#46; pylori</span> virulence factors and GG IL-6 rs1800795 genotype in patients with different types of chronic gastritis&#46;</p>"
        ]
      ]
    ]
    "bibliografia" => array:2 [
      "titulo" => "References"
      "seccion" => array:1 [
        0 => array:2 [
          "identificador" => "bibs0015"
          "bibliografiaReferencia" => array:55 [
            0 => array:3 [
              "identificador" => "bib0280"
              "etiqueta" => "1"
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                0 => array:2 [
                  "contribucion" => array:1 [
                    0 => array:2 [
                      "titulo" => "<span class="elsevierStyleItalic">Helicobacter pylori</span> heterogeneity in patients with gastritis and peptic ulcer disease"
                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => false
                          "autores" => array:7 [
                            0 => "R&#46;I&#46; Armitano"
                            1 => "M&#46;J&#46; Matteo"
                            2 => "C&#46; Goldman"
                            3 => "A&#46; Wonaga"
                            4 => "L&#46;A&#46; Viola"
                            5 => "G&#46;Z&#46; De Palma"
                            6 => "M&#46; Catalano"
                          ]
                        ]
                      ]
                    ]
                  ]
                  "host" => array:1 [
                    0 => array:1 [
                      "Revista" => array:5 [
                        "tituloSerie" => "Infect Genet Evol"
                        "fecha" => "2013"
                        "volumen" => "16"
                        "paginaInicial" => "377"
                        "paginaFinal" => "385"
                      ]
                    ]
                  ]
                ]
              ]
            ]
            1 => array:3 [
              "identificador" => "bib0285"
              "etiqueta" => "2"
              "referencia" => array:1 [
                0 => array:2 [
                  "contribucion" => array:1 [
                    0 => array:2 [
                      "titulo" => "Interleukin-6 genetic variation and susceptibility to gastric cancer in an Iranian population"
                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => false
                          "autores" => array:3 [
                            0 => "M&#46; Attar"
                            1 => "M&#46; Mansoori"
                            2 => "M&#46; Shahbazi"
                          ]
                        ]
                      ]
                    ]
                  ]
                  "host" => array:1 [
                    0 => array:2 [
                      "doi" => "10.22034/APJCP.2017.18.11.3025"
                      "Revista" => array:6 [
                        "tituloSerie" => "Asian Pac J Cancer Prev"
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Article information

ISSN: 03257541
Original language: English

DOI:10.1016/j.ram.2022.04.003

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