Dietary Vitamin B6 intake modulates colonic inflammation in the IL10−/− model of Inflammatory Bowel Disease

Abstract

Pyridoxal‐5‐phosphate, the biologically active form of vitamin B6, serves as a cofactor for over 140 distinct biochemical reactions. Although severe vitamin B6 deficiency is rare, mild inadequacy (plasma PLP < 20 nmol/L) is observed in 19–27% of the US population, depending on age and sex. Plasma PLP concentrations are inversely related to markers of systemic inflammation such as CRP. Furthermore, plasma PLP is depleted in those with inflammatory conditions and, in the case of inflammatory bowel disease (IBD), more so in those with active versus quiescent disease. Restricting B6 intake has been shown to attenuate IBD pathology in mice; however the effects of supplementation are unclear. Thus, we tested the effect of mild inadequacy and moderate supplementation of vitamin B6 on the severity of colonic inflammation in the IL10−/− mouse model of IBD. We observed a bell‐shaped relationship between histologic inflammation and expression of inflammatory mediators (TNFalpha, IL‐6, IFN‐gamma, COX‐2, iNOS), whereby both low and high plasma PLP was associated with a suppression of inflammation. These results raise the possibility that vitamin B6 supplementation might be used to complement existing therapies for the treatment of IBD. Studies to reproduce these results and uncover mechanisms are underway.