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Title: The Salmonella enterica serovar Typhimurium QseB Response Regulator Negatively Regulates Bacterial Motility and Swine Colonization in the Absence of the QseC Sensor Kinase

Author
item Bearson, Bradley - Brad
item Bearson, Shawn
item LEE, IN SOO - Hannam University
item Brunelle, Brian

Submitted to: Microbial Pathogenesis
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/4/2010
Publication Date: 4/22/2010
Citation: Bearson, B.L., Bearson, S.M., Lee, I., Brunelle, B.W. 2010. The Salmonella enterica serovar Typhimurium QseB Response Regulator Negatively Regulates Bacterial Motility and Swine Colonization in the Absence of the QseC Sensor Kinase. Microbial Pathogenesis. 48:214-219.

Interpretive Summary: Salmonella is ubiquitous in the environment. Although in humans the isolation of Salmonella is almost always considered pathogenic, this bacterium can colonize the gastrointestinal tract of non-human hosts without causing clinical disease. This study investigated an environmental signaling system in Salmonella (QseBC) for its role in swine colonization. We found that bacterial motility and swine colonization of Salmonella are dramatically decreased when the environmental sensor (QseC) is inactivated in Salmonella. Detecting environmental signals, especially host signals, are critical for bacteria to survive environmental changes and cause disease. This research has contributed to the knowledge of Salmonella colonization of the swine gastrointestinal tract and will be used by university, industry, and government researchers investigating intervention strategies for Salmonella.

Technical Abstract: Salmonella enterica serovar Typhimurium (S. Typhimurium) responds to the catecholamine, norepinephrine by increasing bacterial growth and enhancing motility. In this study, iron with or without the siderophore, ferrioxamine E also enhanced bacterial motility. Iron-enhanced motility was growth-rate dependent, while norepinephrine-enhanced motility was growth-rate independent. The outer membrane catecholate receptors, IroN, FepA and CirA (required for norepinephrine-enhanced growth) were not required for norepinephrine-enhanced motility, nor was ExbD of the energy-transducing TonB-ExbB-ExbD ferri-siderophore uptake system. Examination of the QseBC two-component system revealed that qseB and qseBC mutants have motility phenotypes similar to wild-type S. Typhimurium, while motility of the qseC mutant was significantly decreased (P<0.01). Each mutant of the QseBC system, as well as mutants of qseE and pmrA, responded to norepinephrine with increased motility, suggesting that other genes are involved in norepinephrine-enhanced motility of S. Typhimurium. In the swine host, fecal shedding of the qseBC mutant was similar to wild-type S. Typhimurium, whereas fecal shedding of the qseC mutant was significantly decreased (P<0.01). Our data indicate that, in a qseC mutant, the QseB response regulator decreases motility and swine colonization; inactivation of the qseBC operon restores these bacterial phenotypes, classifying QseB as a negative regulator of bacterial motility and swine colonization.