Submitted to: Microbial Pathogenesis
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: October 4, 2007
Publication Date: March 20, 2008
Citation: Bearson, B.L., Bearson, S.M. 2008. The role of QseC quorum-sensing sensor kinase in colonization and norepinephrine-enhanced motility of Salmonella enterica serovar Typhirmurium. Microbial Pathogenesis. 44:271-278.
Interpretive Summary: Mammalian cells communicate through hormones. In a similar manner, bacteria produce hormone-like molecules for cell-to-cell communication (termed quorum sensing). Recent literature indicates that cross-talk between these cell communication compounds can occur when bacteria reside in a mammalian host. Thus, hormones such as norepinephrine produced by the host may serve as a signal to bacteria, for example, to trigger invasion gene expression or immune evasion mechanisms. Identifying host compounds that serve as signals to microorganisms during infection may identify targets for intervention of disease and carrier-status (i.e. sub-clinical infections). This study was performed to investigate the response of Salmonella to norepinephrine, since the host stress hormone may trigger Salmonella to reemerge from carrier status in the pig during marketing stress.
This study revealed: 1) exposure of Salmonella to norepinephrine enhances motility of the pathogen; 2) the qseC gene, involved in regulating bacterial quorum sensing, is required for norepinephrine-enhanced motility of Salmonella; and 3) qseC is important for swine colonization because a Salmonella qseC mutant has reduced colonization compared to the wild-type strain.
We have identified a potential strategy for Salmonella intervention. That is, if norepinephrine produced by the pig during stress is a signal for Salmonella to recrudesce from its carrier status, the use of hormone antagonists by swine producers prior to transport may reduce Salmonella shedding incidence. This could impact food safety, since pigs shedding Salmonella are a contamination problem for slaughter plants. Industry, university and government researchers investigating host-pathogen interactions should find this research interesting, especially those analyzing Salmonella in swine.
Transcriptional analysis of Salmonella enterica serovar Typhimurium in the presence of the mammalian hormone Norepinephrine (NE) revealed up-regulation of chemotaxis and motility genes. Motility assays confirmed enhanced motility of wild-type S. Typhimurium in the presence of NE that could be blocked by the a-adrenergic antagonist, phentolamine. Furthermore, a mutation in the qseC gene, encoding the sensor kinase of the two component QseBC quorum sensing system, also diminished NE-enhanced motility in S. Typhimurium. To investigate the role of S. Typhimurium QseC in vivo, thirteen week old pigs were intranasally inoculated with equal concentrations (1 X 109 CFU) of wild-type S. Typhimurium and a qseC mutant. Over a two-week competitive index experiment, the qseC mutant displayed decreased colonization of the gastrointestinal tract compared to the wild-type strain. Thus, this study has identified a correlation in S. Typhimurium between quorum sensing and the regulation by QseBC of colonization and motility in response to norepinephrine. Cross-talk between cell-cell communication systems in Salmonella (quorum sensing) and the host (hormones) may explain opportunistic behaviors of the pathogen during fluctuations of NE levels in vivo, for example, immune evasion as well as stress-induced recrudescence of Salmonella.