Purpose:
Inflammatory bowel disease (IBD) refers to a spectrum of
autoimmune diseases, which result in chronic intestinal
inflammation. Previous findings suggest a role for diet, nutrition and
dysbiosis of the gut microbiota in both the development and progression of the condition.
Vitamin B12 is a key cofactor of
methionine synthase and is produced solely by microbes. Previous work links increased levels of
homocysteine, a substrate of
methionine synthase, MetH, to IBD indicating a potential role for
vitamin B12 deficiency in intestinal injury and
inflammation. This study assessed the role of
vitamin B12 in shaping the gut microbiota and determining responses to intestinal injury using a reproducible murine model of
colitis. Methods: The effects of
vitamin B12 supplementation and deficiency were assessed in vivo; 3-week-old post-weanling C57Bl/6 mice were divided into three dietary treatment groups: (1) sufficient
vitamin B12 (50 mg/Kg), (2) deficient
vitamin B12 (0 mg/Kg) and (3) supplemented
vitamin B12 (200 mg/Kg) for a period of 4 weeks. Intestinal injury was induced with 2%
dextran sodium sulphate (DSS) via
drinking water for 5 days. The impact of varying levels of dietary
vitamin B12 on gut microbiota composition was assessed using
16S rRNA gene sequencing from fecal samples collected at day 0 and day 28 of the dietary intervention, and 7 days following induction of
colitis on day 38, when blood and colonic tissues were also collected. Results: No significant alterations were found in the gut microbiota composition of disease-free animals in response to dietary interventions. By contrast, after DSS-induced
colitis, >30 genera were significantly altered in
vitamin B12 deficient mice. Altered B12 levels produced no significant effect on composite disease-activity scores; however, administration of a B12 deficient diet resulted in reduced DSS-induced epithelial tissue damage. Conclusions:
Vitamin B12 supplementation does not alter the gut microbiota composition under healthy conditions, but does contribute to differential microbial responses and intestinal
dysbiosis following the induction of experimental
colitis.