Role of chemical signaling and auxiliary mechanisms in Salmonella enterica serovar Typhimurium virulence and other enteropathogens

Abstract

Bacterial chemical signaling is a mechanism employed by several bacteria species to interact within surrounding microbiota and their host. Upon this interaction the pathogenic bacteria regulate their virulence traits. The 2-component system QseBC was described on chemical signaling of the Autoinducer-3, epinephrine, and norepinephrine in Salmonella enterica serovar Typhimurium, and a novel branch of pathogenic cascade regulation was raveled. Amongst these mechanisms a novel protein was described, VisP (Virulence and stress-related Periplasmic protein) (29). Its initial role, the interaction with LpxO enzyme (Dioxygenase Fe2+/ ±-ketoglutarate-dependent) and peptoglycan layer was previously shown (29). Further studies are necessary for a complete clarification of these mechanisms, specially related to TTSS encoded both by SPI-1 and SPI-2, and the role of O-antigen from the LPS of S. Typhimurium. Novel mechanisms briefly unveiled by transcriptomic analyses of QseC sensor kinase still need to be assessed. These mechanisms will be further investigated on this project to characterize these mechanisms in human pathogenic bacteria, evaluate their importance, understand novel processes, and validate these results in other members of the Enterobacteriaceae family. The full comprehension of the complex relationship between pathogenic bacteria, the microbiota, and the host is essential subject in microbial pathogenesis. The human intestine albeit a large variety of bacterial species, the majority are commensal bacteria, which suffer the pathogenic bacteria strike from time to time. The chemical signaling among bacteria is the central aspect of this association. The complete elucidation of these signals will be essential to understand their relationship, develop novel technologies and therapies in benefit to human life. (AU)