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

Cell Host Microbe. 2013 Jun 12;13(6):711-22. doi: 10.1016/j.chom.2013.05.013.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

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

Substances

  • IL10 protein, mouse
  • Interleukin-10