A single strain of Clostridium butyricum induces intestinal IL-10-producing macrophages to suppress acute experimental colitis in mice.

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.

• Authors: Atsushi Hayashi, Toshiro Sato, Nobuhiko Kamada, Yohei Mikami, Katsuyoshi Matsuoka, Tadakazu Hisamatsu, Toshifumi Hibi, Axel Roers, Hideo Yagita, Toshiaki Ohteki, Akihiko Yoshimura, Takanori Kanai
• Journal: Cell host & microbe (Cell Host Microbe) Vol. 13 Issue 6 Pg. 711-22 (Jun 12 2013) ISSN: 1934-6069 [Electronic] United States
• PMID: 23768495 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2013 Elsevier Inc. All rights reserved.

Chemical References

• IL10 protein, mouse
• Interleukin-10

Topics

• Animals
• Clostridium Infections (immunology, microbiology, prevention & control)
• Clostridium butyricum (immunology)
• Colitis (immunology, microbiology, prevention & control)
• Disease Models, Animal
• Interleukin-10 (metabolism)
• Intestinal Mucosa (immunology)
• Macrophages (immunology, microbiology)
• Mice
• Mice, Knockout