Evaluation of IL-12 and CXCL-10 in patients with hepatitis C, non-alcoholic fatty liver disease and liver damage for alcohol consumption

• Published in: Annals of hepatology Vol. 27; p. 100865
• Main Authors: Hernandez-Santillan, M, Martínez-Castillo, M, Medina-Ávila, Z, Lemus-Peña, M, Montes de Oca-Ángeles, D, Hernández-Barragan, A, Pérez-Hernández, JL, Higuera-De la Tijera, F, Santana-Vargas, D, Cordero-Pérez, P, Muñoz-Espinoza, L, Córdova-Gallardo, J, Kershenobich, D, Gutiérrez-Reyes, G
• Format: Journal Article
• Language: English
• Published: Elsevier España, S.L.U 01-12-2022; Elsevier
• ISSN: 1665-2681; 2659-5982
• DOI: 10.1016/j.aohep.2022.100865

To Compare serum levels of IL-12 and CXCL-10 in different etiologies of liver disease.
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 subjects control (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.
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).
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, 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 CXCL-10 in advanced stages of the disease, by stimulating and favoring the migration of immune cells to the damage sites.
This work was partially financed by CONACyT SALUD-2016-272579 and PAPIIT- UNAM TA200515.
The authors declare no potential conflicts of interest.