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Vibrio cholerae integrates interspecies quorum-sensing signals to regulate virulence
Vibrio cholerae integrates interspecies quorum-sensing signals to regulate virulence
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Vibrio cholerae integrates interspecies quorum-sensing signals to regulate virulence
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Vibrio cholerae integrates interspecies quorum-sensing signals to regulate virulence
Vibrio cholerae integrates interspecies quorum-sensing signals to regulate virulence

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Vibrio cholerae integrates interspecies quorum-sensing signals to regulate virulence
Vibrio cholerae integrates interspecies quorum-sensing signals to regulate virulence
Journal Article

Vibrio cholerae integrates interspecies quorum-sensing signals to regulate virulence

2025
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Overview
V. cholerae continues to cause sporadic pandemics globally. Although cholera is a self-limiting acute disease, severe cases often require the use of antimicrobials in addition to rehydration therapy. Efforts to eradicate cholera have been hampered by the increased incidence of antimicrobial resistance and low vaccine coverage. The gut chemical environment, driven largely by the microbiota, has been shown to play important roles in modulating colonization by enteric pathogens. Pathogens utilize this chemical environment as cues to optimize virulence and survival. Understanding the underlying mechanisms of pathogen-microbiota interactions may therefore provide avenues to develop control measures targeting virulence and survival. Many of the mechanisms of pathogen-microbiota interactions have yet to be fully described. We demonstrate that V. cholerae integrates interspecies chemical signals (DSFs) produced by members of the microbiota to regulate the expression of important virulence factors. DSFs potently repress the virulence island master regulator (ToxT), effectively attenuating cholera toxin secretion. As other related long-chain fatty acids have been reported to impair ToxT function, and as DSF producers localize to the intestinal crypts and mucus layer, it is likely that V. cholerae employs these signals in a spatial-temporal manner to program the induction and repression of the energy-intensive virulence factors. Our work provides a framework for designing interventions to disrupt this virulence and survival program to control this pathogen.