P31 Prof. Dr. Wree/Prof. Dr. Trautwein
Inflammasome activation during cholestatic liver injury: A trigger of fibrosis progression

We hypothesize that toxic bile acids or cholestasis trigger NLRP3 inflammasome activation, thereby driving cholestatic liver fibrosis. In collaboration with the other inflammasome-focused projects, we plan to identify cell-specific inflammasome components involved in immune-mediated liver injury and study their interaction with hepatic stellate cells. We will analyze bile acid alterations, test the validity of inflammasome components as biomarkers in patients with cholestatic liver disease and apply novel inflammasome inhibitors to stop disease progression.