Abstract

Quorum sensing (QS) plays a vital role in controlling virulence in bacterial species. Vibrio cholerae, the main causative agent of cholera uses chemical signals to control virulence and biofilm formation. QS Always depend on the secretion and detection of signaling molecules known as auto inducers. Contrary to other bacteria that cause virulence at High cell density (HCD) when they attain a specific threshold, reverse is the case for V. Cholerae. At Low cell density (LCD), activation in the expression of virulence gene by V. cholerae destabilizes HapR while stabilizing AphA. The activation of AphA structural genes result in the expression of CT and TCP virulence together with the formation of biofilm. At HCD, the coherence of the two quorum-sensing auto-inducers (CAI-1 and AI-2) represses the expression of the virulence genes by activating HapR which in turn synthesizes Hap protease that acts as a detachase to get rid of the virulence genes and biofilm formation. In this review, we outline the QS mechanism used by Vibrio cholerae to cause infection by the production of virulence factors. In addition, we examine how this infection can be minimize through the use of chemicals which act as either inhibitors or agonist to the QS system.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call