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World J Gastroenterol. Mar 21, 2010; 16(11): 1321-1329
Published online Mar 21, 2010. doi: 10.3748/wjg.v16.i11.1321
Alcoholic liver disease and the gut-liver axis
Gyongyi Szabo, Shashi Bala
Gyongyi Szabo, Shashi Bala, Liver Center, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, United States
Author contributions: Szabo G and Bala S worked together on the concept and outline of the article and the specific chapters were written by one of the authors in equal distribution.
Supported by NIAAA Grants No. AA017729 and No. AA011576
Correspondence to: Gyongyi Szabo, MD, PhD, Professor, Liver Center, Department of Medicine, University of Massachusetts Medical School, LRB 215, Worcester, MA 01605, United States. gyongyi.szabo@umassmed.edu
Telephone: +1-508-8565275 Fax: +1-508-8564770
Received: January 5, 2010
Revised: February 10, 2010
Accepted: February 17, 2010
Published online: March 21, 2010
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.

Keywords: Kupffer cell, Gut permeability, microRNA, Tumor necrosis factor-α, Endotoxin