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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U2 - 10.1016/j.chom.2013.05.013
DO - 10.1016/j.chom.2013.05.013
M3 - Article
C2 - 23768495
AN - SCOPUS:84879109909
VL - 13
SP - 711
EP - 722
JO - Cell Host and Microbe
JF - Cell Host and Microbe
SN - 1931-3128
IS - 6
ER -