Modulation of tumor necrosis factor receptors 1 and 2 in chronic hepatitisB and C: The differences and implications in pathogenesis

Tumor necrosis factor (TNF) plays a role in the pathogenesis of chronic hep atitis B (CHB) and chronic hepatitis C (CHC). The difference in the cytokin e responses between hepatitis B virus (HBV) and hepatitis C virus (HCV) inf ections may have implications in the pathogenesis of these diseases. We per formed a comparative study to examine the possible differences in the TNF-T NF receptor (TNFR) response between CHB and CHC. We studied the cytokine le vels of 38 patients with CHB, 40 patients with CHC and 9 patients with dual hepatitis B and C, and compared them with the baseline levels of 12 health y controls. The plasma levels of TNF-alpha, interferon-gamma, interleukin ( IL)-2, IL-4, IL-10 and soluble TNFR-1 and 2 (sTNFR-1 and 2) were quantified by enzyme-linked immunosorbent assays. The expression of TNFR-1 and 2 in r iver tissues was examined in 30 cases of CHB and 15 cases of CHC by semiqua ntitative reverse transcription polymerase chain reaction. The results show ed that sTNFR-1 revels correlated with liver inflammation in all patients, whereas this correlation was not found with sTNFR-2 or other cytokines. Liv er inflammation indicators were higher in HCV RNA(+) than in HCV RNA- CHC. Most significantly, sTNFR-1 levels correlated with liver inflammation in CH B, but not in CHC. However, the expression of TNFR-1 and 2 in liver was sim ilar between CHB and CHC. These findings suggest that the TNFR signal trans duction pathway is modulated differently in HBV and HCV infection. Copyrigh t (C) 2001 National Science Council, ROC and S. Karger AG, Basel.