P-49 CONCENTRATION OF IL-12 AND CXCL-10 IN CHRONIC LIVER DISEASES

Hernandez-Santillan, Marisela; Martínez-Castillo, Moisés; Medina-Ávila, Zaira; Hernández-Barragan, Abigail; Lemus-Peña, María; de Oca-Ángeles, Daniel Montes; Pérez-Hernández, José Luis; Higuera-De la Tijera, Fátima; Santana-Vargas, Daniel; Montalvo-Jave, Eduardo; Cordero-Pérez, Paula; Muñoz-Espinoza, Linda; Córdova-Gallardo, Jacqueline; Torre-Delgadillo, Aldo; Gutiérrez-Reyes, Gabriela

doi:10.1016/j.aohep.2023.100949

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This study aimed to compare serum levels of IL-12 and CXCL-10 in different etiologies of liver disease. Materials and MethodsA cross-sectional and multicenter study was carried out, including subjects with alcoholism according to criteria WHO, without (OH) and with liver injury (cirrhosis, CiOH) and (Alcoholic Hepatitis, HA); non-alcoholic fatty liver (NAFLD) and chronic Hepatitis C (CHC), diagnosed by clinical, biochemical data. They were compared with control subjects (CT). For determination of IL-12 and CXCL-10 with Multiplex®-MERCK©. Statistical analysis by SPSS V.22 using U de Mann Whitney, p<0.05; values expressed as mean ± standard error. ResultsIncluded 20 subjects with NAFLD, 78 CHC, 14 HA, 20 CiOH, 15 OH y 60 CT. IL-12 was found elevated in OH, HA, CHC vs. CT in OH vs. HCc y HGNA (p≤0.05). CXCL-10 was found elevated in CiOH, HA, and CHC vs. CT(p≤0.050). ConclusionsThe IL-12 showed elevated levels in subjects with alcohol consumption and CHC vs. CT that activates other cell types involved in inflammation. CXCL-10 is induced by IFN-γ and was found elevated in CiOH, HA and CHC, exerting their biological effects through CXCR3, including activation of peripheral immune cells and apoptosis. The ratio of IL-12/CXCL-10 in OH increased 4.6 times, ratifying the participation in chronic and continual inflammatory response by alcohol consumption. IL-12 and CXCL-10 have an important role in alcohol-induced liver disease, confirming their contribution to inflammation, being evident in CXCL-10 in advanced stages of the disease by stimulating and favoring the migration of immune cells to the damage sites. FundingThis work was partially financed by CONACyT SALUD-2016-272579 and PAPIIT- UNAM TA200515." 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ISSN: 1665-2681

Annals of Hepatology (AoH) is an international, open access journal published bi-monthly with funds from the Fundación Clínica Médica Sur. It is the official journal of the Mexican Association of Hepatology (AMH), the Latin American Association for the Study of the Liver (ALEH), the Canadian Association for the Study of the Liver (CASL) and the Czech Society of Hepatology (CSH). AoH publishes editorials, opinions, concise reviews, original articles, brief reports, letters to the editor, news from affiliated associations, clinical practice guidelines and summaries of congresses in the field of Hepatology.

Topics covered by AoH include alcoholic liver disease, autoimmune hepatitis, biliary diseases, drug-induced liver injury, genetic liver diseases, NAFLD/NASH and viral hepatitis (HAV, HBV, HCV, HDV, HEV). Our journal seeks to publish articles on basic clinical care and translational research focused on preventing rather than treating the complications of end-stage liver disease.

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Marisela Hernandez-Santillan1, Moisés Martínez-Castillo1, Zaira Medina-Ávila1, Abigail Hernández-Barragan1, María Lemus-Peña1, Daniel Montes de Oca-Ángeles1, José Luis Pérez-Hernández2, Fátima Higuera-De la Tijera2, Daniel Santana-Vargas2, Eduardo Montalvo-Jave2, Paula Cordero-Pérez3, Linda Muñoz-Espinoza3, Jacqueline Córdova-Gallardo4, Aldo Torre-Delgadillo1,5, Gabriela Gutiérrez-Reyes1

1 Liver, Pancreas and Motility Laboratory, Unit of Research in Experimental Medicine, School of Medicine, National Autonomy University of México (UNAM), Mexico City, Mexico

2 Department of Gastroenterology, General Hospital of México “Dr. Eduardo Liceaga,” Mexico City, Mexico

3 Universitary Hospital “Dr. José Eluterio González”, School of Medicine, Autonomy University of Nuevo León (UANL), Nuevo Leon, Mexico City, Mexico

4 General Hospital “Dr. Manuel Gea González”, Mexico City, Mexico

5 National Institute of Medical Sciences and Nutrition “Salvador Zubirán,” Mexico City, Mexico

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Abstract

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This article is part of special issue:

Vol. 28. Issue S1

Abstracts of the 2022 Annual Meeting of the ALEH

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Introduction and Objectives

Chronic liver diseases are characterized by persistent inflammation related to high production of cytokines such as IL-12 and chemokine CXCL-10/IP-10 that attract activated Th1 lymphocytes that increase the production of IFN-g and TNF-a, perpetuating the inflammatory cascade. This study aimed to compare serum levels of IL-12 and CXCL-10 in different etiologies of liver disease.

Materials and Methods

A cross-sectional and multicenter study was carried out, including subjects with alcoholism according to criteria WHO, without (OH) and with liver injury (cirrhosis, CiOH) and (Alcoholic Hepatitis, HA); non-alcoholic fatty liver (NAFLD) and chronic Hepatitis C (CHC), diagnosed by clinical, biochemical data. They were compared with control subjects (CT). For determination of IL-12 and CXCL-10 with Multiplex®-MERCK©. Statistical analysis by SPSS V.22 using U de Mann Whitney, p<0.05; values expressed as mean ± standard error.

Results

Included 20 subjects with NAFLD, 78 CHC, 14 HA, 20 CiOH, 15 OH y 60 CT. IL-12 was found elevated in OH, HA, CHC vs. CT in OH vs. HCc y HGNA (p≤0.05). CXCL-10 was found elevated in CiOH, HA, and CHC vs. CT(p≤0.050).

Conclusions

The IL-12 showed elevated levels in subjects with alcohol consumption and CHC vs. CT that activates other cell types involved in inflammation. CXCL-10 is induced by IFN-γ and was found elevated in CiOH, HA and CHC, exerting their biological effects through CXCR3, including activation of peripheral immune cells and apoptosis. The ratio of IL-12/CXCL-10 in OH increased 4.6 times, ratifying the participation in chronic and continual inflammatory response by alcohol consumption. IL-12 and CXCL-10 have an important role in alcohol-induced liver disease, confirming their contribution to inflammation, being evident in CXCL-10 in advanced stages of the disease by stimulating and favoring the migration of immune cells to the damage sites.

Funding

This work was partially financed by CONACyT SALUD-2016-272579 and PAPIIT- UNAM TA200515.

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