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Microbial metabolite butyrate facilitates M2 macrophage polarization and function
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Journal Article
Microbial metabolite butyrate facilitates M2 macrophage polarization and function
2016
Overview
Metabolites from intestinal microbes modulate the mucosal immune system by regulating the polarization and expansion of T cells. Whether the microbial metabolites influence macrophage polarization, however, is poorly understood. Here, we show that the large bowel microbial fermentation product, butyrate, facilitates M2 macrophage polarization,
in vitro
and
in vivo
. The supernatant from butyrate-treated M2 macrophage increased the migration and enhanced the wound closure rate of MLE-12 cells. Butyrate attenuated intestinal inflammation in mice with dextran sulfate sodium (DSS)-induced colitis, with a significant increase in colonic expression of the M2 macrophage-associated protein, Arg1. M2 macrophage treated with butyrate, had increased activation of the H3K9/STAT6 signaling pathway, suggesting a mechanism for butyrate facilitated M2 macrophage polarization. Collectively, our study indicated that commensal microbe-derived butyrate is a novel activator of STAT6-mediated transcription through H3K9 acetylation driving M2 macrophage polarization and delineated new insights into the immune interplay underlying inflammatory bowel disease.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 13/1
/ 13/31
/ 38
/ 38/77
/ 64
/ 64/60
/ Animals
/ Chemotaxis, Leukocyte - immunology
/ Colitis
/ Colitis - chemically induced
/ Colon
/ Dextran
/ Dextran Sulfate - adverse effects
/ Female
/ Histone Deacetylases - metabolism
/ Humanities and Social Sciences
/ Intestinal Mucosa - immunology
/ Intestinal Mucosa - metabolism
/ Intestinal Mucosa - microbiology
/ Macrophage Activation - immunology
/ Mice
/ Rodents
/ Science
/ Sodium
/ STAT6 Transcription Factor - metabolism
/ Sulfates
/ Wounds
