28-Feb-19
Non-alcoholic fatty liver disease (NAFLD) is characterised by the accumulation of excess fat in the liver, termed steatosis. NAFLD encompasses simple steatosis and its inflammatory state called non-alcoholic steatohepatitis (NASH) which is a core driver of liver cirrhosis, and hepatocellular carcinoma (HCC). This project will focus on the role of interferon lambdas (IFN-λs) on the progression of liver inflammation and fibrosis.
 
Interferon lambda (IFN-λ) is a central antiviral cytokine in the liver that is elevated in NASH, and that contributes to the progression of liver inflammation and fibrosis. The mechanism of IFN-λ induction, and cells involved however, remain unknown. We hypothesise that microbial ligands originating from the gut, enter the liver in the portal blood and stimulate IFN-λ expression. This project will aim to determine the contribution and identity of intestinal biota that stimulate IFN-λ, the responsive cells, and the mechanisms by which IFN-λ drives liver inflammation. We will utilise cutting edge genomics, primary cell culture, flow cytometry and molecular biology techniques to shed some light on the role of IFN-λ in NASH. This study will pave the way for future treatments aimed at halting the progression of inflammation in NASH.

Student level: PhD
Supervisor: Professor Golo Ahlenstiel