On or Off: Life-Changing Decisions Made by Vibrio cholerae Under Stress

Abstract

Vibrio cholerae , the causative agent of the infectious disease, cholera, is commonly found in brackish waters and infects human hosts via the fecal-oral route. V. cholerae is a master of stress resistance as V. cholerae's dynamic lifestyle across different physical environments constantly exposes it to diverse stressful circumstances. Specifically, V. cholerae has dedicated genetic regulatory networks to sense different environmental cues and respond to these signals. With frequent outbreaks costing a tremendous amount of lives and increased global water temperatures providing more suitable aquatic habitats for V. cholerae , cholera pandemics remain a probable catastrophic threat to humanity. Understanding how V. cholerae copes with different environmental stresses broadens our repertoire of measures against infectious diseases and expands our general knowledge of prokaryotic stress responses. In this review, we summarize the regulatory mechanisms of how V. cholerae fights against stresses in vivo and in vitro.

Non-O1/Non-O139 Vibrio cholerae—An Underestimated Foodborne Pathogen? An Overview of Its Virulence Genes and Regulatory Systems Involved in Pathogenesis

“…After oral ingestion, pathogenic bacteria will encounter a set of host-derived defense systems, including chemical and biological barriers, when entering the stomach and arriving at the small intestine. Therefore, various genes involved in adaptation processes as a response to these conditions can be found in NOVCs to ensure that they reach the small intestine to interact with epithelial cells [40,41]. The stage 1 section therefore describes the adaptation to low pH values in the stomach [41,42]; the adaptation to reactive nitrogen and oxygen species in the stomach [43,44]; changes in porin channel size to prevent the diffusion of harmful molecules into the bacterial cell such as bile salts from the gallbladder in the duodenum [45]; efflux pumps to displace harmful molecules such as bile in the duodenum and antimicrobial peptides in the small intestine [46]; the formation of protective biofilms to protect bacteria against antimicrobial substances from the stomach, duodenum, and the small intestine; and the T6SS to compete with the predominant gut microbiome [47].…”

“…Therefore, various genes involved in adaptation processes as a response to these conditions can be found in NOVCs to ensure that they reach the small intestine to interact with epithelial cells [40,41]. The stage 1 section therefore describes the adaptation to low pH values in the stomach [41,42]; the adaptation to reactive nitrogen and oxygen species in the stomach [43,44]; changes in porin channel size to prevent the diffusion of harmful molecules into the bacterial cell such as bile salts from the gallbladder in the duodenum [45]; efflux pumps to displace harmful molecules such as bile in the duodenum and antimicrobial peptides in the small intestine [46]; the formation of protective biofilms to protect bacteria against antimicrobial substances from the stomach, duodenum, and the small intestine; and the T6SS to compete with the predominant gut microbiome [47]. All mechanisms and genes involved in stage 1 are shown in orange in Figure 1.…”