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. Author manuscript; available in PMC: 2018 Jul 5.
Published in final edited form as: Cell Metab. 2017 Jun 15;26(1):110–130. doi: 10.1016/j.cmet.2017.05.008

Fig. 1. Intestinal bacteria convert dietary nutrients to immunomodulatory metabolites.

Fig. 1

Polysaccharides that cannot be digested by host enzymes, such as cellulose, are metabolized by the intestinal microbiota to short-chain fatty acids (SCFAs, green). These exert a plethora of anti-inflammatory effects, such as inducing the expansion and de novo differentiation of regulatory T cells; enhancing the barrier function of the intestinal mucosa through epithelial cells and goblet cells; facilitating production of antibodies by B cells; inhibiting the maturation of dendritic cells and promoting an anti-inflammatory phenotype; and reducing production of pro-inflammatory cytokines by innate immune cells. Dietary tryptophan is degraded to indole derivatives (blue). Indoles promote epithelial barrier function, e.g. by supporting the maintenance of type 3 innate lymphoid cells, which are the primary producers of IL-22. Dietary arginine is metabolized to polyamines (red), which promote the integrity of the intestinal epithelium and reduce the production of pro-inflammatory cytokines by macrophages. See text for details. DC, dendritic cell; EC, epithelial cell; GC, goblet cell; ILC3, type 3 innate lymphoid cell; MΦ, macrophage; NΦ, neutrophil; Treg, regulatory T cell.