Role of tumor necrosis factor-α, interleukin-1β, interleukin-6 in liver inflammation in chronic hepatitis B and chronic hepatitis C

Introduction Hepatitis B (HBV) and hepatitis C (HCV) viruses are important health problems because they cause serious consequences such as chronic hepatitis, cirrhosis, fulminant hepatitis, and hepatocellular carcinoma (HCC) (1). Chronic liver disease occurs as a result of the relationship between a progressive wound healing process and inflammatory response (2). The mechanism of persistent and progressive HBV infection is not clear yet, and it is thought that host immune and genetic factors may play an important role (3). Cytokines play a fundamental role in the immunopathogenesis of HBV infection and may affect the susceptibility to HBV infection and the natural course of the infection (4). HCV infection stimulates the production of inflammatory cytokines and chemokines, resulting in hepatic inflammation and chronic hepatitis (5). Many cytokines that affect the progression of liver disease and play an important role in the fibrotic process have been reported. Cytokines can reduce viral replication and control the host immune response. Accordingly, it can be said that the serum level of cytokines affects the outcome of the disease (6). DOI: 10.4274/gulhane.galenos.2021.1338 ORIGINAL ARTICLE