Vibrio cholerae high cell density quorum sensing activates the host intestinal innate immune response

Quorum sensing fundamentally alters the interaction of Vibrio cholerae with aquatic environments, environ-mental hosts, and the human intestine. At high cell density, the quorum-sensing regulator HapR represses not only expression of cholera toxin and the toxin co-regulated pilus, virulence factors essential in human infection, but also synthesis of the Vibrio polysaccharide (VPS) exopolysaccharide-based matrix required for abiotic and biotic surface attachment. Here, we describe a feature of V. cholerae quorum sensing that shifts the host-pathogen interaction toward commensalism. By repressing pathogen consumptive anabolic metabolism and, in particular, tryptophan uptake, V. cholerae HapR stimulates host intestinal serotonin pro-duction. This, in turn, activates host intestinal innate immune signaling to promote host survival.

Automated summary

Quorum sensing alters the interaction between Vibrio cholerae and its environment and hosts, leading to a commensal relationship with the host. By regulating gene expression and metabolism, quorum sensing promotes survival of the host by activating the host's intestinal immune signaling.