Salmonella exploits a quorum-sensing family signal of the gut commensal Stenotrophomonas maltophilia to facilitate its colonization.

چکیده اصلی

Successful colonization by enteric pathogens requires overcoming colonization resistance of the native microbiota while tightly regulating the expression of energetically-expensive virulence factors. Here we describe a feedback mechanism by which the enteric pathogen Salmonella orchestrates this balance through environmental manipulation. We show that Salmonella-induced oxidative stress can stimulate the colonic resident Stenotrophomonas maltophilia to enhance the secretion of the diffusible signal factor cis-2-hexadecenoic acid (c2-HDA), a potent repressor of Salmonella virulence. By sensing this metabolite, Salmonella can attenuate its own virulence program to favor proliferation and colonic colonization. In murine models, Salmonella colonization was significantly enhanced in the colon, and inflammation reduced, in the presence of c2-HDA produced by S. maltophilia. Moreover, the ability of Salmonella to recognize c2-HDA within the murine colon was crucial for its successful colonization. These findings reveal a pathogen-commensal signaling axis through which pathogen-driven inflammatory cues reshape the metabolic output of the microbiota, generating regulatory signals that are co-opted to optimize pathogen fitness in the gut.

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