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 +CD11cint 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.
| Original language | English |
|---|---|
| Pages (from-to) | 711-722 |
| Number of pages | 12 |
| Journal | Cell Host and Microbe |
| Volume | 13 |
| Issue number | 6 |
| DOIs | |
| Publication status | Published - 2013 Jun 12 |
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ASJC Scopus subject areas
- Immunology and Microbiology(all)
- Cancer Research
- Molecular Biology
Cite this
A single strain of Clostridium butyricum induces intestinal IL-10-producing macrophages to suppress acute experimental colitis in mice. / Hayashi, Atsushi; Sato, Toshiro; Kamada, Nobuhiko; Mikami, Yohei; Matsuoka, Katsuyoshi; Hisamatsu, Tadakazu; Hibi, Toshifumi; Roers, Axel; Yagita, Hideo; Ohteki, Toshiaki; Yoshimura, Akihiko; Kanai, Takanori.
In: Cell Host and Microbe, Vol. 13, No. 6, 12.06.2013, p. 711-722.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - A single strain of Clostridium butyricum induces intestinal IL-10-producing macrophages to suppress acute experimental colitis in mice
AU - Hayashi, Atsushi
AU - Sato, Toshiro
AU - Kamada, Nobuhiko
AU - Mikami, Yohei
AU - Matsuoka, Katsuyoshi
AU - Hisamatsu, Tadakazu
AU - Hibi, Toshifumi
AU - Roers, Axel
AU - Yagita, Hideo
AU - Ohteki, Toshiaki
AU - Yoshimura, Akihiko
AU - Kanai, Takanori
PY - 2013/6/12
Y1 - 2013/6/12
N2 - 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 +CD11cint 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.
AB - 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 +CD11cint 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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UR - http://www.scopus.com/inward/citedby.url?scp=84879109909&partnerID=8YFLogxK
U2 - 10.1016/j.chom.2013.05.013
DO - 10.1016/j.chom.2013.05.013
M3 - Article
VL - 13
SP - 711
EP - 722
JO - Cell Host and Microbe
JF - Cell Host and Microbe
SN - 1931-3128
IS - 6
ER -