Abstract
Alcoholic liver disease (ALD) is one of the leading causes of liver diseases and liver-related death worldwide. Of the many factors that contribute to the pathogenesis of ALD, gut-derived lipopolysaccharide (LPS) plays a central role in induction of steatosis, inflammation, and fibrosis in the liver. In this review, we discuss the mechanisms by which alcohol contributes to increased gut permeability, the activation of Kupffer cells, and the inflammatory cascade by LPS. The role of the Toll-like receptor 4 (TLR4) complex in LPS recognition and the importance of the TLR4-induced signaling pathways are evaluated in ALD.
2010 Baishideng. All rights reserved.
Publication types
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Research Support, N.I.H., Extramural
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Review
MeSH terms
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Animals
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Central Nervous System Depressants / pharmacology
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Endotoxins / pharmacology
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Ethanol / pharmacology
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Gastrointestinal Tract / drug effects
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Gastrointestinal Tract / microbiology
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Gastrointestinal Tract / pathology
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Gastrointestinal Tract / physiopathology*
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Humans
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Lipopolysaccharides / pharmacology
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Liver / cytology
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Liver / drug effects
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Liver / pathology
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Liver / physiopathology*
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Liver Diseases, Alcoholic / pathology
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Liver Diseases, Alcoholic / physiopathology*
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MicroRNAs / genetics
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MicroRNAs / metabolism
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Signal Transduction / drug effects
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Toll-Like Receptor 4 / metabolism
Substances
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Central Nervous System Depressants
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Endotoxins
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Lipopolysaccharides
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MicroRNAs
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Toll-Like Receptor 4
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Ethanol