AI Article Synopsis
- Quorum sensing in Vibrio cholerae influences its behavior in both aquatic environments and the human intestine, especially at high cell densities.
- High cell density triggers the HapR regulator, which reduces the synthesis of key virulence factors like cholera toxin and the Vibrio polysaccharide, essential for attachment and infection.
- This regulation promotes a commensal relationship by enhancing host intestinal serotonin production, which activates immune signaling and supports host survival.
Article 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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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9534793 | PMC |
| http://dx.doi.org/10.1016/j.celrep.2022.111368 | DOI Listing |
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