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Role of innate immunity and the microbiota in liver fibrosis: crosstalk between the liver and gut
Author(s) -
Seki Ekihiro,
Schnabl Bernd
Publication year - 2012
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2011.219691
Subject(s) - steatohepatitis , alcoholic liver disease , innate immune system , liver disease , fibrosis , immunology , biology , liver injury , fatty liver , immune system , medicine , pathology , cirrhosis , disease
Liver fibrosis occurs as a wound‐healing scar response following chronic liver inflammation including alcoholic liver disease, non‐alcoholic steatohepatitis, viral hepatitis, cholestatic liver disease and autoimmune liver diseases. The liver has a unique vascular system within the gastrointestinal tract, as the majority of the liver's blood supply comes from the intestine through the portal vein. When the intestinal barrier function is disrupted, an increase in intestinal permeability leads to the translocation of intestine‐derived bacterial products such as lipopolysaccharide (LPS) and unmethylated CpG containing DNA to the liver via the portal vein. These gut‐derived bacterial products stimulate innate immune receptors, namely Toll‐like receptors (TLRs), in the liver. TLRs are expressed on Kupffer cells, endothelial cells, dendritic cells, biliary epithelial cells, hepatic stellate cells, and hepatocytes. TLRs activate these cells to contribute to acute and chronic liver diseases. This review summarizes recent studies investigating the role of TLRs, intestinal microbiota and bacterial translocation in liver fibrosis, alcoholic liver disease and non‐alcoholic steatohepatitis.