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Microbial metabolite butyrate facilitates M2 macrophage polarization and function.

Ji J, Shu D, Zheng M, Wang J, Luo C, Wang Y, Guo F, Zou X, Lv X, Li Y, Liu T, Qu H - Sci Rep (2016)

Bottom Line: Metabolites from intestinal microbes modulate the mucosal immune system by regulating the polarization and expansion of T 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.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.

View Article: PubMed Central - PubMed

Affiliation: Institute of Animal Science, Guangdong Academy of Agricultural Sciences, 1 Dafeng 1st Street, Wushan, Tianhe District, Guangzhou 510640, China.

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus

Butyrate promotes IL-4-induced STAT6 signaling pathways in M2 macrophage.M2-BMDMs were incubated with IL-4 and IL-4 with butyrate for the indicated time periods. Cell lysates were prepared and blotted with anti-phospho-STAT6. Total STAT6 and β-actin were probed as quantitative controls. Data are representative of three independent experiments.
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f5: Butyrate promotes IL-4-induced STAT6 signaling pathways in M2 macrophage.M2-BMDMs were incubated with IL-4 and IL-4 with butyrate for the indicated time periods. Cell lysates were prepared and blotted with anti-phospho-STAT6. Total STAT6 and β-actin were probed as quantitative controls. Data are representative of three independent experiments.

Mentions: STAT6 is a critical transcription factor for the IL-4-mediated signaling response in M2 macrophage polarization21, therefore, we compared phosphorylation of STAT6 in butyrate-treated M2-BMDMs and untreated M2-BMDMs. We observed an increase in STAT6 phosphorylation in response to IL-4 in butyrate-treated M2-BMDMs compared with M2-BMDMs (Fig. 5). Therefore, the higher expression of M2 macrophage marker mRNA may be a consequence of increased STAT6 phosphorylation.


Microbial metabolite butyrate facilitates M2 macrophage polarization and function.

Ji J, Shu D, Zheng M, Wang J, Luo C, Wang Y, Guo F, Zou X, Lv X, Li Y, Liu T, Qu H - Sci Rep (2016)

Butyrate promotes IL-4-induced STAT6 signaling pathways in M2 macrophage.M2-BMDMs were incubated with IL-4 and IL-4 with butyrate for the indicated time periods. Cell lysates were prepared and blotted with anti-phospho-STAT6. Total STAT6 and β-actin were probed as quantitative controls. Data are representative of three independent experiments.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4837405&req=5

f5: Butyrate promotes IL-4-induced STAT6 signaling pathways in M2 macrophage.M2-BMDMs were incubated with IL-4 and IL-4 with butyrate for the indicated time periods. Cell lysates were prepared and blotted with anti-phospho-STAT6. Total STAT6 and β-actin were probed as quantitative controls. Data are representative of three independent experiments.
Mentions: STAT6 is a critical transcription factor for the IL-4-mediated signaling response in M2 macrophage polarization21, therefore, we compared phosphorylation of STAT6 in butyrate-treated M2-BMDMs and untreated M2-BMDMs. We observed an increase in STAT6 phosphorylation in response to IL-4 in butyrate-treated M2-BMDMs compared with M2-BMDMs (Fig. 5). Therefore, the higher expression of M2 macrophage marker mRNA may be a consequence of increased STAT6 phosphorylation.

Bottom Line: Metabolites from intestinal microbes modulate the mucosal immune system by regulating the polarization and expansion of T 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.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.

View Article: PubMed Central - PubMed

Affiliation: Institute of Animal Science, Guangdong Academy of Agricultural Sciences, 1 Dafeng 1st Street, Wushan, Tianhe District, Guangzhou 510640, China.

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus