ARS | Publication request: The QseB Response Regulator is Required for Decreased Bacterial Motility and Swine Colonization in a QseC Mutant of Salmonella enterica serovar Typhimurium

Submitted to: Meeting Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: February 20, 2009
Publication Date: May 21, 2009
Citation: Bearson, B.L., Bearson, S.M., Lee, I., Brunelle, B.W. 2009. The QseB Response Regulator is Required for Decreased Bacterial Motility and Swine Colonization in a QseC Mutant of Salmonella enterica serovar Typhimurium [abstract]. In: Abstracts of the 109th General Meeting of the American Society for Microbiology, May 17-21, 2009, Philadelphia, Pennsylvania. p. 611.

Technical Abstract: Inactivation of the QseC (PreB) sensor kinase decreases the motility of a qseC mutant compared to wild-type Salmonella enterica serovar Typhimurium (S. Typhimurium). In addition, the competitive fitness of the qseC mutant for colonization of the swine gastrointestinal tract is decreased compared to the wild-type strain. Therefore, the QseC sensor kinase enhances both bacterial motility and competitive fitness. To assess the role of the QseB (PreA) response regulator in bacterial motility and Salmonella colonization in swine, S. Typhimurium strains were constructed to knock out the qseB gene and the qseBC operon. Whereas the qseC mutant had decreased motility compared to wild-type S. Typhimurium, the qseB and qseBC mutants had motility phenotypes similar to wild-type S. Typhimurium. To determine the colonization potential of a qseBC mutant in the swine gastrointestinal tract compared to the qseC mutant and wild-type S. Typhimurium, 7-week old piglets (n=5 per strain) were intranasally inoculated with the S. Typhimurium strains. Fecal shedding of the bacterial strains was monitored for 7 days post-inoculation (dpi) using quantitative and qualitative Salmonella culturing methods. Swine fecal shedding of the qseBC mutant was similar to wild-type S. Typhimurium over the 7-day period. In contrast, fecal shedding of the qseC mutant was significantly decreased at 2, 3, 5, and 7 dpi compared to wild-type S. Typhimurium and at 2, 3, and 5 dpi compared to the qseBC mutant (P<0.01). Our data indicate that the presence of the QseB response regulator in a qseC mutant decreases bacterial motility and swine colonization, and inactivation of the qseBC operon restores these bacterial phenotypes similar to wild-type S. Typhimurium. These results suggest that QseB is a negative regulator of genes involved in bacterial motility and swine colonization.