2011/11/29 by Ekihiro Seki, Bernd Schnabl · 436 citations
Medicine · Nursing · #Alcoholic liver disease #Biology #Cirrhosis #Clinical Nutrition and Gastroenterology #Disease #Fatty liver #Fibrosis #Immune system #Immunology #Innate immune system #Internal medicine #Liver Disease Diagnosis and Treatment #Liver disease #Liver injury #Liver physiology and pathology #Medicine #Pathology #Steatohepatitis
paper · open access · doi:10.1113/jphysiol.2011.219691
published in The Journal of Physiology 590(3), 447-458 (Wiley)
openalex publication_date 2011/11/29 · openalex created_date 2025/10/10 · openalex updated_date 2026/08/06
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.