Efficient responses to host and bacterial signals during Vibrio cholerae colonization

Abstract

Vibrio cholerae, the microorganism responsible for the diarrheal disease cholera, is able to sense and respond to a variety of changing stimuli in both its aquatic and human gastrointestinal environments. Here we present a review of research efforts aimed toward understanding the signals this organism senses in the human host. V. cholerae's ability to sense and respond to temperature and pH, bile, osmolarity, oxygen and catabolite levels, nitric oxide, and mucus, as well as the quorum sensing signals produced in response to these factors will be discussed. We also review the known quorum sensing regulatory pathways and discuss their importance with regard to the regulation of virulence and colonization during infection.

Keywords: V. cholerae; bile; colonization; environmental signals; mucus; pH; quorum sensing; virulence.

Figure 1. Environmental signals alter V. cholerae virulence. A variety of environmental signals, including pH, temperature, bile, mucus, nitric oxide, and quorum sensing, alter the transcriptional program of V. cholerae, ensuring that virulence factors are produced at the optimal point of the infectious cycle.

Figure 2. Quorum sensing circuits in V. cholerae. At low cell density, the membrane proteins CqsS and LuxQ act as kinases to initiate transfer of phosphate through LuxU to LuxO. LuxO-P, with σ⁵⁴ of RNA polymerase, serve as a transcription factor to produce qrr1–4. Qrr1–4 and Hfq inhibit HapR. At high cell density,^- CqsS and LuxO, through the binding of AI molecules, act as phosphatases to reverse the flow of phosphate through the regulatory circuit. LuxO becomes deactivated, qrr1–4 expression becomes repressed, and HapR is expressed.^,-