Hepatitis B virus-mediated sodium influx contributes to hepatic inflammation via synergism with intrahepatic danger signals

Hepatitis B virus-mediated sodium influx contributes to hepatic inflammation via synergism with intrahepatic danger signals

Blog Article

Summary: The NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome has been involved in the pathogenesis of various chronic liver diseases.However, its role in hepatitis B virus (HBV)-associated hepatitis remains unknown.Here we demonstrate the synergistic effect of HBV with potential intrahepatic danger signals on NLRP3 inflammasome activation.HBV exposure at the appropriate temporal points enhances potassium efflux-dependent NLRP3 inflammasome activation in Counter Height Table macrophages and also increases NLRP3 inflammasome-mediated inflammation in HBV-transgenic mouse model.HBV-mediated synergism with intrahepatic signals represented by ATP molecules on NLRP3 activation was observed via relevance analysis, confocal microscopy, and co-immunoprecipitation, and its effector cytokines exhibit positive associations with hepatic inflammation in patients with severe hepatitis ADVANCED B COMPLEX B.

Furthermore, the synergism of HBV on NLRP3 inflammasome activation owes to increased sodium influx into macrophages.Our data demonstrate that HBV contributes to hepatic inflammation via sodium influx-dependent synergistic activation of NLRP3 inflammasome, which provides a deeper understanding of immune pathogenesis in HBV-associated hepatitis.