QseB mediates biofilm formation and invasion in Salmonella enterica serovar Typhi.

Abstract

QseB is a response regulator of the QseBC two-component system (TCS) which is associated with quorum sensing and functions as a global regulator of flagella, biofilm formation, and virulence. The function of QseB and its interaction with QseC has been the subject of study in some organisms, however, little work was done in Salmonella enterica serovar Typhi (S. Typhi). The objective of this study was to investigate the effect of QseB on biofilm formation and virulence in S. Typhi. It showed that the biofilm formation ability of qseC mutant was limited as compared to the wild type strain. We also show overexpression of qseB was in a qseC mutant. Interestingly, deletion of qseB in a qseC mutant restored a wild type phenotype. These results suggested that QseB may account for the impaired biofilm formation in the absence of QseC. Furthermore, deletion of qseB in wild type cells decreased biofilm formation, whereas overexpression of qseB in wild type cells increased biofilm formation. Quantitative real-time PCR also revealed the up-regulation of some fimbria-associated genes in a qseB overexpression strain. These results indicate that QseB may enhance biofilm formation in the presence of QseC. Taken together, we hypothesize that QseB has dual regulatory functions which are dependent upon its cognate sensor. Additionally, invasion of HeLa cells was enhanced in qseB mutant but attenuated in a qseC mutant compared with wild-type. The β-galactosidase activity of invF::lacZ was increased in qseB mutant but decreased in qseC mutant which was consistent with invasion results. In conclusion, QseB may have dual regulatory functions concerning biofilm formation and plays a negative role in virulence of S. Typhi.