Alcoholic liver disease and the gut-liver axis

被引:417
作者
Szabo, Gyongyi [1 ]
Bala, Shashi [1 ]
机构
[1] Univ Massachusetts, Sch Med, Dept Med, Ctr Liver, Worcester, MA 01605 USA
关键词
Kupffer cell; Gut permeability; microRNA; Tumor necrosis factor-alpha; Endotoxin; LIPOPOLYSACCHARIDE-BINDING-PROTEIN; TUMOR-NECROSIS-FACTOR; CACO-2 CELL MONOLAYER; TOLL-LIKE RECEPTOR-4; TNF-ALPHA PRODUCTION; RAT KUPFFER CELLS; NF-KAPPA-B; HEPATIC NEUTROPHIL INFILTRATION; ACETALDEHYDE-INDUCED INCREASE; GRAM-NEGATIVE BACTERIA;
D O I
10.3748/wjg.v16.i11.1321
中图分类号
R57 [消化系及腹部疾病];
学科分类号
100201 [内科学];
摘要
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. (C) 2010 Baishideng. All rights reserved.
引用
收藏
页码:1321 / 1329
页数:9
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