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The participation of an infant harbored bacterial commensal in urea nitrogen salvaging

Breast milk often promotes the establishment of commensal communities dominated by bifidobacteria within the developing neonate. This is driven by infant‐indigestible molecules such as soluble glycans secreted in milk referred to as human milk oligosaccharides. Accordingly, concentrations of protein are lower in human milk relative to other mammals, which may be inadequate to satisfy increased nitrogen demands during postnatal growth, let alone the metabolic requirements of resident colonic commensals. Interestingly, urea accounts for 15% of total nitrogen in human breast milk, representing a potential nitrogen reservoir for both the infant and its harbored microbiota. We hypothesize that urea nitrogen salvaging (UNS) is a critical host‐commensal metabolic interaction that is modulated by Bifidobacterium longum subsp. infantis (B. infantis) that are a frequent early colonizers of the nursing infant gut. The B. infantis genome encodes a urease gene cluster underlying its urea hydrolysis phenotype to enable these commensals to utilize urea as a sole nitrogen source. This is consistent with B. infantis participation in UNS within the infant gut along with gene expression profiles while differentially shunting nitrogen through catabolic and anabolic pathways. Moreover, we have determined that B. infantis are auxotrophic for L‐cysteine and utilize this amino acid as a sole nitrogen source under non‐limiting conditions. This is suggestive of coupled nitrogen and sulfur metabolism in the breastfed infant gut, and may reflect the evolutionary trajectory of infant‐borne bifidobacterial lineages.