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Review
. 2019 Apr 17:6:48.
doi: 10.3389/fnut.2019.00048. eCollection 2019.

Metabolism of Dietary and Microbial Vitamin B Family in the Regulation of Host Immunity

Ken Yoshii  1   2 , Koji Hosomi  1 , Kento Sawane  1   3   4 , Jun Kunisawa  1   2   3   5   6   7
Affiliations
Review

Metabolism of Dietary and Microbial Vitamin B Family in the Regulation of Host Immunity

Ken Yoshii et al. Front Nutr. .

Abstract

Vitamins are micronutrients that have physiological effects on various biological responses, including host immunity. Therefore, vitamin deficiency leads to increased risk of developing infectious, allergic, and inflammatory diseases. Since B vitamins are synthesized by plants, yeasts, and bacteria, but not by mammals, mammals must acquire B vitamins from dietary or microbial sources, such as the intestinal microbiota. Similarly, some intestinal bacteria are unable to synthesize B vitamins and must acquire them from the host diet or from other intestinal bacteria for their growth and survival. This suggests that the composition and function of the intestinal microbiota may affect host B vitamin usage and, by extension, host immunity. Here, we review the immunological functions of B vitamins and their metabolism by intestinal bacteria with respect to the control of host immunity.

Keywords: absorption; gut microbiota; intestinal immunity; nutrition; vitamin.

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Figures

Figure 1
Figure 1
Vitamin B1 and B2-mediated immunometabolism in B cell differentiation in the intestine. Vitamin B1 acts as a cofactor for enzymes such as pyruvate dehydrogenase and α-ketoglutarate dehydrogenase that are involved in the TCA cycle. Vitamin B2 acts as a cofactor for enzymes such as succinate dehydrogenase in the TCA cycle and acyl-CoA dehydrogenase in fatty acid oxidation (FAO, also known as β-oxidation). Naïve B cells preferentially use the TCA cycle for efficient energy generation. Once B cells are activated to differentiate into IgA-producing plasma cells, they utilize glycolysis for the production of IgA antibody.
Figure 2
Figure 2
Regulation of MAIT cells by microbial metabolites derived from vitamin B2 and B9. Commensal bacteria/pathogens produce the vitamin B2 metabolite 6-hydroxymethyl-8-D-ribityllumazine. It binds to major histocompatibility complex (MHC) related protein (MR1) on antigen-presenting cells, which activate mucosal associated invariant T (MAIT) cells to promote the production of inflammatory cytokines such as IFN-γ and IL-17. These reactions contribute to defense against pathogens and conversely are associated with inflammation. In contrast, the vitamin B9 metabolite acetyl-6-formylpterin binds as an antagonist to MR1, thus inhibiting the activation of MAIT cells.
Figure 3
Figure 3
Pivotal roles of vitamins B3, B7, and B9 in maintenance of immunological homeostasis. Vitamin B3 binds to GPR109a in dendritic cells and macrophages, and GPR109a signaling leads to an increase in anti-inflammatory properties, resulting in differentiation into regulatory T cells (Treg). Vitamin B7 binds to histones and, by histone biotinylation, suppresses the secretion of pro-inflammatory cytokines. Once naïve T cells differentiate into Treg cells, they highly express folate receptor 4 (FR4). Consistent with this finding, vitamin B9 is required for the survival of Treg cells.
Figure 4
Figure 4
Schematic representation of B-vitamin-mediated interaction between commensal bacteria and host immunity.
See this image and copyright information in PMC

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