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. 2016 May 15;310(10):G822-31.
doi: 10.1152/ajpgi.00440.2015. Epub 2016 Mar 24.

Butyrate enhances antibacterial effects while suppressing other features of alternative activation in IL-4-induced macrophages

Maria R Fernando  1 , Alpana Saxena  1 , José-Luis Reyes  1 , Derek M McKay  2
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Butyrate enhances antibacterial effects while suppressing other features of alternative activation in IL-4-induced macrophages

Maria R Fernando et al. Am J Physiol Gastrointest Liver Physiol. .
Free article

Abstract

The short-chain fatty acid butyrate is produced by fermentation of dietary fiber by the intestinal microbiota; butyrate is the primary energy source of colonocytes and has immunomodulatory effects. Having shown that macrophages differentiated with IL-4 [M(IL-4)s] can suppress colitis, we hypothesized that butyrate would reinforce an M(IL-4) phenotype. Here, we show that in the presence of butyrate M(IL-4)s display reduced expression of their hallmark markers Arg1 and Ym1 and significantly suppressed LPS-induced nitric oxide, IL-12p40, and IL-10 production. Butyrate treatment likely altered the M(IL-4) phenotype via inhibition of histone deacetylation. Functionally, M(IL-4)s treated with butyrate showed increased phagocytosis and killing of bacteria, compared with M(IL-4) and this was not accompanied by enhanced proinflammatory cytokine production. Culture of regulatory T cells with M(IL-4)s and M(IL-4 + butyrate)s revealed that both macrophage subsets suppressed expression of the regulatory T-cell marker Foxp3. However, Tregs cocultured with M(IL-4 + butyrate) produced less IL-17A than Tregs cocultured with M(IL-4). These data illustrate the importance of butyrate, a microbial-derived metabolite, in the regulation of gut immunity: the demonstration that butyrate promotes phagocytosis in M(IL-4)s that can limit T-cell production of IL-17A reveals novel aspects of bacterial-host interaction in the regulation of intestinal homeostasis.

Keywords: innate immunity; intestinal homeostasis; microbiota.

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