期刊
CELL HOST & MICROBE
卷 19, 期 2, 页码 227-239出版社
CELL PRESS
DOI: 10.1016/j.chom.2016.01.003
关键词
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资金
- NIH [K08 DK081830, R01 AA020703, U01 AA021856]
- Biomedical Laboratory Research & Development Service of the VA Office of Research and Development [I01BX002213]
- UCSD School of Medicine Microscopy Core Grant [P30 NS047101]
Approximately half of all deaths from liver cirrhosis, the tenth leading cause of mortality in the United States, are related to alcohol use. Chronic alcohol consumption is accompanied by intestinal dysbiosis and bacterial overgrowth, yet little is known about the factors that alter the microbial composition or their contribution to liver disease. We previously associated chronic alcohol consumption with lower intestinal levels of the antimicrobial-regenerating islet-derived (REG)-3 lectins. Here, we demonstrate that intestinal deficiency in REG3B or REG3G increases numbers of mucosa-associated bacteria and enhances bacterial translocation to the mesenteric lymph nodes and liver, promoting the progression of ethanol-induced fatty liver disease toward steatohepatitis. Overexpression of Reg3g in intestinal epithelial cells restricts bacterial colonization of mucosal surfaces, reduces bacterial translocation, and protects mice from alcohol-induced steatohepatitis. Thus, alcohol appears to impair control of the mucosa-associated microbiota, and subsequent breach of the mucosal barrier facilitates progression of alcoholic liver disease.
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