Infection leaves a genetic and functional mark on the gut population of a commensal bacterium

Gastrointestinal infection changes microbiome composition and gene expression. In this study, we demonstrate that enteric infection also promotes rapid genetic adaptation in a gut commensal. Measurements of Bacteroides thetaiotaomicron population dynamics within gnotobiotic mice reveal that these populations are relatively stable in the absence of infection, and the introduction of the enteropathogen Citrobacter rodentium reproducibly promotes rapid selection for a single-nucleotide variant with increased fitness. This mutation promotes resistance to oxidative stress by altering the sequence of a protein, IctA, that is essential for fitness during infection. We identified commensals from multiple phyla that attenuate the selection of this variant during infection. These species increase the levels of vitamin B6 in the gut lumen. Direct administration of this vitamin is sufficient to significantly reduce variant expansion in infected mice. Our work demonstrates that a self-limited enteric infection can leave a stable mark on resident commensal populations that increase fitness during infection. [Display omitted] •Infection induces a rapid selective sweep in gut populations of B. thetaiotaomicron•A single point mutation is sufficient to increase commensal fitness during inflammation•Commensals modulate population dynamics by altering vitamin levels in the gut Gastrointestinal infection profoundly impacts the intestinal environment. Tawk et al. show that gut commensals can respond to transient infection through mutation and selection. Infection-induced selective sweeps largely replace existing commensal populations with inflammation-adapted variants, and metabolites from other commensal species can modulate these dynamics.