Abstract

Introduction & Aims: Alcoholic liver disease (ALD) represents the hepatic manifestation of alcohol overconsumption and includes a clinical spectrum ranging from alcoholic fatty liver, alcoholic steatohepatitis (ASH), progressive liver fibrosis to cirrhosis and hepatocellular carcinoma. The translocation of pathogen-associated molecular patterns (PAMPs, i.e. LPS, microbial DNA) from the gut to the liver is considered an important pathomechanism in the development of ASH. Once in the liver, PAMPs will activate numerous pathways that promote hepatic steatosis, inflammation and fibrosis. An intact gut barrier is maintained by a continuous interaction between the gut microbiota and the mucosal immune system. Specific members of the gut microbiota such as Akkermansia muciniphila convey protective properties by affecting mucosal thickness and reducing portal and systemic LPS levels.

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