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Toll‐like receptors in alcoholic liver disease, non‐alcoholic steatohepatitis and carcinogenesis
Author(s) -
Roh Yoon Seok,
Seki Ekihiro
Publication year - 2013
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/jgh.12019
Subject(s) - steatohepatitis , medicine , alcoholic liver disease , toll like receptor , fatty liver , chronic liver disease , innate immune system , fibrosis , hepatocellular carcinoma , receptor , liver disease , lipopolysaccharide , hepatic stellate cell , immune system , immunology , cancer research , disease , cirrhosis
Activation of innate immune systems including Toll‐like receptor ( TLR ) signaling is a key in chronic liver disease. Recent studies suggest that gut microflora‐derived bacterial products (i.e. lipopolysaccharide [ LPS ], bacterial DNA ) and endogenous substances (i.e. high‐mobility group protein B1 [ HMGB 1], free fatty acids) released from damaged cells activate hepatic TLR s that contribute to the development of alcoholic ( ASH ) and non‐alcoholic steatohepatitis ( NASH ) and liver fibrosis. The crucial role of TLR 4, a receptor for LPS , has been implicated in the development of ASH , NASH , liver fibrosis, and hepatocellular carcinoma. However, the role of other TLR s, such as TLR 2 and TLR 9 in chronic liver disease remains less clear. In this review, we will discuss the role of TLR 2, 4, and 9 in K upffer cells and hepatic stellate cells in the development of ASH , NASH , and hepatocarcinogenesis.