Vibrio cholerae high cell density quorum sensing activates the host intestinal innate immune response
0301 basic medicine
Cholera Toxin
Serotonin
Virulence Factors
Tryptophan
Quorum Sensing
Cell Count
Gene Expression Regulation, Bacterial
Article
Immunity, Innate
3. Good health
Intestines
03 medical and health sciences
Bacterial Proteins
Polysaccharides
Humans
Vibrio cholerae
DOI:
10.1016/j.celrep.2022.111368
Publication Date:
2022-09-20T14:48:30Z
AUTHORS (6)
ABSTRACT
Quorum sensing fundamentally alters the interaction of Vibrio cholerae with aquatic environments, environmental 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 production. This, in turn, activates host intestinal innate immune signaling to promote host survival.
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