Biotin is an essential
vitamin and critical cofactor in several metabolic pathways, and its deficiency has been linked to several disorders including
inflammatory bowel disease (IBD). We previously reported that
biotin deficiency (BD) in mice, whether modeled through intestine-specific deletion of
biotin transporter (SMVT-icKO) or through a
biotin-deficient diet, resulted in intestinal
inflammation consistent with an IBD-like phenotype. To assess whether the gut microbiome is associated with these BD-induced changes, we collected stool and intestinal samples from both of these mouse models and utilized them for
16S rRNA gene sequencing. We find that both diet-mediated and deletion-mediated BD result in the expansion of opportunistic microbes including Klebsiella, Enterobacter, and Helicobacter, at the expense of mucus-resident microbes including Akkermansia. Additionally, microbiome
dysbiosis resulting from diet-mediated BD precedes the onset of the IBD-like phenotypic changes. Lastly, through the use of predictive metagenomics, we report that the resulting BD-linked microbiome perturbations exhibit increased
biotin biosynthesis in addition to several other perturbed metabolic pathways. Altogether, these results demonstrate that
biotin deficiency results in a specific microbiome composition, which may favor microbes capable of
biotin synthesis and which may contribute to intestinal
inflammation.