The putative sensor kinase QseC of Salmonella enterica serovar Typhi can promote invasion in the presence of glucose

Salmonella enterica serovar Typhi (S. Typhi) causes a human-restricted systemic infection called typhoid fever. It invades intestinal epithelial cells requiring expression of genes located at SPI-1. QseC is a regulator of quorum sensing that initiates transcription of a series of flagellar genes in reponse to AI-3 in Escherichia coli. By sequencing analysis, we have found that the homolog of the putative qseBC (t3098, t3099) in a wild-type strain of S. Typhi shares 98% and 99% identity with that of S. enterica serovar Typhimurium (S. Typhimurium), respectively. Glucose is not only an energy source compound but also an important environmental signaling molecule for enteropathogenic bacteria. In this study, we found that a series of invasion-associated genes in SPI-1 were downregulated in the qseC mutant of S. Tyhpi compared to the wild-type in the presence of glucose, by the genomic microarray assay. Results of qRT-PCR were consistent with the microarray data and suggest that the transcriptional regulation of invasion-associated genes by QseC is glucose-dependent and the regulation is not dependent on QseB. A qseC mutant cultured in the presence of glucose condition was impaired in invasion of epithelial cells. These data indicate that QseC can promote invasion in S. Typhi in the presence of glucose.