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Anti‐inflammatory strategies in alcoholic steatohepatitis
Author(s) -
Enomoto Nobuyuki,
Takei Yoshiyuki,
Yamashina Shunhei,
Ikejima Kenichi,
Kitamura Tsuneo,
Sato Nobuhiro
Publication year - 2007
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/j.1440-1746.2006.04652.x
Subject(s) - steatohepatitis , kupffer cell , medicine , proinflammatory cytokine , alcoholic liver disease , priming (agriculture) , alcoholic hepatitis , fatty liver , inflammation , immunology , biology , disease , cirrhosis , germination , botany
The hepatotoxic effects of alcohol have been described in detail, but mechanisms underlying the hepatotoxicity have been only partially characterized. Recently, increasing lines of evidence indicate that Kupffer cells play multiple roles in initiation and progression of alcoholic steatohepatitis. After ethanol exposure, Kupffer cells are activated via a mechanism dependent on gut‐derived endotoxin, and release active mediators such as proinflammatory cytokines and eicosanoids. These mediators are responsible for the pathophysiology of alcoholic steatohepatitis. This review discusses the current concept of Kupffer cell‐mediated steatohepatitis and how it relates to the hypothesis on the mechanism by which alcoholic steatohepetitis is caused, as well as several key issues that have to be addressed in this field: (i) How do Kupffer cells undergo priming and activation during alcoholic steatohepatitis?; (ii) What kind of mediators are involved?; and (iii) How does the concept translate into a strategy for therapeutics of alcoholic steatohepatitis?