| Literature DB >> 23768495 |
Atsushi Hayashi1, Toshiro Sato, Nobuhiko Kamada, Yohei Mikami, Katsuyoshi Matsuoka, Tadakazu Hisamatsu, Toshifumi Hibi, Axel Roers, Hideo Yagita, Toshiaki Ohteki, Akihiko Yoshimura, Takanori Kanai.
Abstract
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.Entities:
Mesh:
Substances:
Year: 2013 PMID: 23768495 DOI: 10.1016/j.chom.2013.05.013
Source DB: PubMed Journal: Cell Host Microbe ISSN: 1931-3128 Impact factor: 21.023