Hepatitis C virus pathogenesis: Serum IL-33 level indicates liver damage

Hepatitis C virus (HCV) is one of the major causes of chronic liver disease in the world. Majority of infected individuals are unable to clear the virus and as consequence of infection, cirrhosis and hepatocellular carcinoma can be developed in later stages. Immune system cells secrete cytokines which play a crucial role in intercellular communication system responsible for immune response. Interleukine-33 (IL-33) is a new member of the IL-1 family. It plays a key role in Th2-cells differentiation, activating mast cells and promotes dendritic cells development in bone marrow culture. IL-33 Pro-inflammatory properties are detrimental in inflammatory bowel disease (IBD), allergic contact dermatitis and other several experimental models of inflammation. In this study we examined the concentrations of serum IL-33 in patients with chronic hepatitis C (CHC) and healthy controls (C) to evaluate the potential role of IL-33 in the pathogenic process of CHC. We determined the concentrations of serum IL-33 and its correlation to the HCV virus activity and the degree of liver fibrosis. We indicated the liver viability by measuring liver enzymes and serum zinc levels. We found that IL-33 response is correlated positively to the increase of liver enzymes and degree of liver fibrosis which indicate its important role in the pathogenesis of CHC and its association with the severity of liver injury in CHC patients.