QseC MediatesSalmonella entericaSerovar Typhimurium VirulenceIn VitroandIn Vivo

• DOI: 10.1128/iai.01038-09
• Publication Date: 2009-12-23T02:10:09Z
• Authors: Cristiano G. Moreira; David Weinshenker; Vanessa Sperandio
• Keywords: Salmonella enterica; Pathogenicity island; Virulence factor

The autoinducer-3 (AI-3)/epinephrine (Epi)/norepinephrine (NE) interkingdom signaling system mediates chemical communication between bacteria and their mammalian hosts. three signals are sensed by the QseC histidine kinase (HK) sensor. Salmonella enterica serovar Typhimurium is a pathogen that uses HKs to sense its environment regulate virulence. invades epithelial cells survives within macrophages. Invasion of mediated type III secretion (T3SS) encoded in pathogenicity island 1 (SPI-1), while macrophage survival systemic disease T3SS SPI-2. Here we show plays an important role pathogenicity. A qseC mutant was impaired flagellar motility, invasion cells, macrophages attenuated for infection 129x1/SvJ mice. acts globally, regulating expression genes SPI-1 SPI-2 vitro vivo (during mice). Additionally, dopamine beta-hydroxylase knockout (Dbh(-)(/)(-)) mice do not produce Epi or NE showed different susceptibility than wild-type These data suggest AI-3/Epi/NE key factor during pathogenesis vivo. Elucidation this should contribute better understanding complex interplay host infection.