期刊
JOURNAL OF HEPATOLOGY
卷 39, 期 1, 页码 68-76出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/S0168-8278(03)00186-7
关键词
alcohol; liver; cytokines; galactosamine; mice
Background/Aims: Alcohol sensitizes the liver to several injuries. The mechanisms leading to this sensitization are poorly defined. In the present study, we developed a mouse model of chronic exposure to alcohol vapours that sensitize mice to galactosamine (GAL) liver injury. Methods: C57BL/6 mice were exposed to ethanol vapours for 10 days. Liver injury was induced by intraperitoneal injection of GAL (1 g/kg) and mice were killed 24 It later. Results: GAL challenge after ethanol pre-treatment significantly raised serum alanine aminotransaminase (ALT) levels and enhanced liver inflammation when compared with the controls (GAL alone). Serum keratinocyte chemoattractant (KC) and monocyte chemoattractant protein-1 (MCP-1) levels were significantly increased in the GAL + ethanol group. On the contrary, serum interleukin 10 (IL-10) levels were lower than in controls. Anti-KC, antitumour necrosis factor alpha antibodies and intestinal decontamination significantly protected mice from liver injury. In GAL + ethanol-treated mice, IL-10 treatment reduced ALT release, KC and MCP-1 serum and hepatic mRNA levels, and improved liver inflammation. Conclusions: Enhancement of GAL-induced liver injury by ethanol is associated with an imbalance between proinflammatory cytokines and the anti-inflammatory cytokine IL-10 and depends on gut bacterial flora. (C) 2003 European Association for the Study of the Liver. Published by Elsevier Science B.V. All rights reserved.
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