Background and aim: During chronic Hepatitis C (CHC) is generates persistent inflammation that can progress to fibrosis. IL-1β is responsible for the initiation of inflammation, the action of IL-1β, its activity is regulated by IL-1RA which has also been implicated in the liver in cell proliferation. IFN-γ is the main initiating agents of the antiviral response, additionally promotes the production of CXCL-10 / IP-10 activating the chemotaxis of lymphocytes and NK cells. Objective. To evaluate the serum levels IL-1β, IL-1RA, IFN-γ and CXCL-10 in patients with CHC and its association with liver fibrosis.
Material and methods: A cross-sectional study, patients with CHC without comorbidities with grade of fibrosis for Fibroscan/Fibrotest and control group (CT) were included. Subjects CT with negative viral panel and without signs of liver disease. The quantification of IL-1β, IL-1RA, IFN-γ and CXCL-10 molecules in serum the multiple suspension method. Statistical analysis was performed using Mann-Whitney U test, p<0.05 was considered significant. All patients signed informed consent. Protocol approved by the General Hospital of Mexico (HG/ DI/16/107/03/082) and UNAM (FMD/DI/15/2019).
Results: CHC (107) and CT (192) subjects were include. The concentration (pg/mL) of IL-1β was 7±2 for CHC and 3±0.1 for CT (p=0.048), of IL-1RA was 44±11 for CHC and 50±13 for CT (p=0.734). The serum levels of IFN-γ 9±4 for CHC, and for CT 11±3 (p=0.002). In the case of CXCL-10, 938±92 for of CHC and 361±21 for the CT (p<0.001). Comparing by grade of fibrosis for IL-1β, no significant difference was found. IL-1RA showed differences in F1vsF4 and F3vsF4. The IFN-γ in F1vsF4 and F2vsF4. Finally, CXCL-10, presented significance only in F1vsF4.
Conclusions: Higher levels of IL-1β and CXCL10 were found in HCc, as part of the active inflammatory response. Whereas in the comparison of fibrosis stages: IFN-γ and CXCL-10 showed participation in early stages. On the other hand, IL-1β does not display changes, however, their antagonist IL-1RA increases in F4 suggesting their participation in liver regeneration.
This work was partially financed by CONACyT SALUD-2016-272579 and PAPIIT- UNAM TA200515.
Conflicts of interest: The authors have no conflicts of interest to declare.
