Editorial
Is Helicobacter pylori a new kid on the block?
¿Es el Helicobacter pylori un recién llegado?
a Department of Pharmacology, Toxicology and Therapeutic Chemistry, Faculty of Pharmacy and Food Sciences and Institute of Biomedicine of the University of Barcelona (IBUB), University of Barcelona, Barcelona, Spain
b Spanish Biomedical Research Center in Diabetes and Associated Metabolic Diseases (CIBERDEM)-Instituto de Salud Carlos III, Madrid, Spain
c Pediatric Research Institute-Hospital Sant Joan de Déu, Esplugues de Llobregat, Spain
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"tieneTextoCompleto" => true "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "78" "paginaFinal" => "79" ] ] "autores" => array:1 [ 0 => array:3 [ "autoresLista" => "Manuel Vázquez-Carrera" "autores" => array:1 [ 0 => array:4 [ "nombre" => "Manuel" "apellidos" => "Vázquez-Carrera" "email" => array:1 [ 0 => "mvazquezcarrera@ub.edu" ] "referencia" => array:3 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] 2 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">c</span>" "identificador" => "aff0015" ] ] ] ] "afiliaciones" => array:3 [ 0 => array:3 [ "entidad" => "Department of Pharmacology, Toxicology and Therapeutic Chemistry, Faculty of Pharmacy and Food Sciences and Institute of Biomedicine of the University of Barcelona (IBUB), University of Barcelona, Barcelona, Spain" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Spanish Biomedical Research Center in Diabetes and Associated Metabolic Diseases (CIBERDEM)-Instituto de Salud Carlos III, Madrid, Spain" "etiqueta" => "b" "identificador" => "aff0010" ] 2 => array:3 [ "entidad" => "Pediatric Research Institute-Hospital Sant Joan de Déu, Esplugues de Llobregat, Spain" "etiqueta" => "c" "identificador" => "aff0015" ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "¿Es el <span class="elsevierStyleItalic">Helicobacter pylori</span> un recién llegado?" ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">It is well known that traditional risk factors for atherosclerosis, such as age, smoking, diabetes mellitus, dyslipidemia, hypertension, and chronic inflammation, only account for approximately 50% of the incidence of atherosclerosis.<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">1</span></a> Therefore, identifying new risks factors that contribute to atherosclerosis development may help to better recognize people with a high cardiovascular risk in the early stages of the disease. <span class="elsevierStyleItalic">Helicobacter pylori</span> infection has been recently identified as a potential atherosclerotic risk factor.<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">2</span></a><span class="elsevierStyleItalic">H. pylori</span> is a gram-negative bacterium that colonizes the stomach of approximately half of the world's population. This infection is a major cause of several gastric diseases and it also increases the risk of gastric cancer.<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">3</span></a> However, since this bacterial infection produces not only local inflammation, but also systemic inflammation, <span class="elsevierStyleItalic">H. pylori</span> infection has also been linked to many extra-gastrointestinal manifestations, including atherosclerosis.<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">2</span></a> In fact, recent evidence indicate that <span class="elsevierStyleItalic">H. pylori</span> infection is involved in the initiation, progression and complication of the atherosclerotic plaque through several mechanisms. Thus, it has been reported that a positive correlation exists between <span class="elsevierStyleItalic">H. pylori</span> infection and the increase in carotid intima-media thickness (CIMT).<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">2</span></a> This parameter is obtained by measuring the thickness of the inner and middle layers of the carotid artery and is used as a marker of subclinical and asymptomatic atherosclerotic. In addition, the systemic inflammation caused by chronic <span class="elsevierStyleItalic">H. pylori</span> infection may accelerate atherosclerotic plaque formation. Likewise, this bacterial infection can destroy gastric parietal cells, which secrete intrinsic factor, a key factor involved in vitamin B<span class="elsevierStyleInf">12</span> absorption, ultimately leading to deficiency of this vitamin. As a result of this deficiency, the enzyme methionine synthase is inhibited, causing an increase in homocysteine that promotes atherosclerosis. Finally, <span class="elsevierStyleItalic">H. pylori</span> infection may precipitate dyslipidemia and the release of cytoxin-associated gene A (CagA) by <span class="elsevierStyleItalic">H. pylori</span>-infected cells promotes foam cell formation.</p><p id="par0010" class="elsevierStylePara elsevierViewall">Although many studies have reported a positive correlation between <span class="elsevierStyleItalic">H. pylori</span> infection and atherosclerosis, this correlation remains controversial since some studies do not support it.<a class="elsevierStyleCrossRefs" href="#bib0085"><span class="elsevierStyleSup">4,5</span></a> In this issue of Clínica e Investigación en Arteriosclerosis, Baspinar O. et al. address this subject by examining the presence of subclinical atherosclerosis by measuring CIMT in patients without comorbid disease and positive or negative for <span class="elsevierStyleItalic">H. pylori</span> infection. In agreement with previous studies,<a class="elsevierStyleCrossRefs" href="#bib0075"><span class="elsevierStyleSup">2,6</span></a> the authors observed that CIMT was increased in patients infected with <span class="elsevierStyleItalic">H. pylori</span> compared with those not infected, indicating the presence of subclinical atherosclerosis in these patients. Moreover, CIMT increased with the bacterial density in endoscopic biopsy material, reinforcing the presence of a positive relationship between <span class="elsevierStyleItalic">H. pylori</span> infection and CIMT. The patients infected with <span class="elsevierStyleItalic">H. pylori</span> studied did not show dyslipidemia or vitamin B<span class="elsevierStyleInf">12</span> deficiency, thereby demonstrating that these alterations did not contribute to subclinical atherosclerosis associated with <span class="elsevierStyleItalic">H. pylori</span> infection.</p><p id="par0015" class="elsevierStylePara elsevierViewall">Interestingly, the authors of this study also found that patients infected with <span class="elsevierStyleItalic">H. pylori</span> exhibited increased levels of growth differentiation factor 15 (GDF-15) and that a significant correlation was found between GDF-15 and CIMT, while no significant correlation was observed between these parameters and other studied atherosclerosis markers. GDF-15 is a stress-induced cytokine with circulating serum GDF-15 levels in healthy subjects ranging from 200 to 1000<span class="elsevierStyleHsp" style=""></span>pg/mL, but these levels are remarkably elevated under conditions of cellular stress such as in several diseases (especially in cancer, cardiovascular disease, obesity, mitochondrial diseases, and aging).<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">7</span></a> In fact, the presence of increased levels of this cytokine in subjects suffering many of these diseases has led GDF-15 to be considered as a biomarker of these pathologies, being associated with overall mortality. In this line, GDF-15 is a reliable biomarker in patients with stable and acute coronary artery disease.<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">8</span></a> However, GDF-15 has been reported to protect against aging-mediated systemic inflammatory responses<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">9</span></a> and to mediate anti-inflammatory effects in mice with acute myocardial infarction.<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">10</span></a> The finding that serum GDF-15 concentration is positively associated with atherosclerosis, as reported by Baspinar O. et al., agrees with a previous recent study conducted in Japanese individuals aged 60–69 years.<a class="elsevierStyleCrossRef" href="#bib0120"><span class="elsevierStyleSup">11</span></a> The mechanism responsible for this association remains unknown. However, since GDF-15 deficiency attenuates macrophage activity,<a class="elsevierStyleCrossRef" href="#bib0125"><span class="elsevierStyleSup">12</span></a> individuals with higher levels of GDF-15 might have increased macrophage activity. As macrophages play an important role in atherosclerosis development,<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">13</span></a> this could indicate that patients with increased circulating levels of GDF-15 are at higher risk of developing atherosclerosis. In addition, since inflammatory cytokines induce the expression of GDF-15, cytokine release caused by endothelial dysfunction or by <span class="elsevierStyleItalic">H. pylori</span> infection could be the mechanism underlying the increase in GDF-15. Further studies are needed to evaluate whether serum GDF-15 concentrations are an earlier marker for subclinical atherosclerosis that could help us to estimate the risk of atherosclerosis.</p><p id="par0020" class="elsevierStylePara elsevierViewall">In conclusion, the study by Baspinar O. et al. provides new evidence supporting that <span class="elsevierStyleItalic">H. pylori</span> infection may exacerbate atherosclerosis. However, further studies are needed before establishing its place among classical risk factors of atherosclerosis. If finally confirmed, strategies to eradicate <span class="elsevierStyleItalic">H. pylori</span> might contribute to reduce the incidence of atherosclerosis. Moreover, this study also highlights the potential role of GDF-15 as a biomarker for subclinical atherosclerosis that might allow preventive strategies to be instituted early in the disease process. However, the use of GDF-15 as a biomarker might be challenging since GDF-15 is regulated by many factors, including body weight, age, thyroid hormone activity, and drug treatment, among others. Therefore, although promising, additional studies should confirm the potential of GDF-15 as a biomarker for atherosclerosis.</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflict of interest</span><p id="par0025" class="elsevierStylePara elsevierViewall">The authors declare that they have no conflict of interest.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:2 [ 0 => array:2 [ "identificador" => "sec0005" "titulo" => "Conflict of interest" ] 1 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0015" "bibliografiaReferencia" => array:13 [ 0 => array:3 [ "identificador" => "bib0070" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Atherosclerosis" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:6 [ 0 => "P. 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| Year/Month | Html | Total | |
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| 2024 November | 4 | 0 | 4 |
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