期刊
CELL HOST & MICROBE
卷 13, 期 6, 页码 711-722出版社
CELL PRESS
DOI: 10.1016/j.chom.2013.05.013
关键词
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资金
- Japanese Ministry of Education, Culture, Sports, Science, and Technology
- Japanese Ministry of Health, Labour and Welfare
- Keio University Medical Fund
- Miyarisan Pharmaceutical
- Japan Society for the Promotion of Science for Young Scientist
- Grants-in-Aid for Scientific Research [24659375, 24689036, 23590949] Funding Source: KAKEN
Imbalance in gut bacterial composition provokes host proinflammatory responses causing diseases such as colitis. Colonization with a mixture of Clostridium species from clusters IV and XIVa was shown to suppress colitis through the induction of IL-10-producing regulatory T (Treg) cells. We demonstrate that a distinct Clostridium strain from cluster I, Clostridium butyricum (CB), prevents acute experimental colitis in mice through induction of IL-10, an anti-inflammatory cytokine. However, while CB treatment had no effect on IL-10 production by T cells, IL-10-producing F4/80(+)CD11b(+)CD11c(int) macrophages accumulated in the inflamed mucosa after CB treatment. CB directly triggered IL-10 production by intestinal macrophages in inflamed mucosa via the TLR2/MyD88 pathway. The colitis-preventing effect of CB was negated in macrophage-specific IL-10-deficient mice, suggesting that induction of IL-10 by intestinal macrophages is crucial for the probiotic action of CB. Collectively, CB promotes IL-10 production by intestinal macrophages in inflamed mucosa, thereby preventing experimental colitis in mice.
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