Contribution of the stg fimbrial operon of Salmonella enterica serovar Typhi during interaction with human cells

Department of Microbiology and Immunology, University of Montreal, C.P. 6128 Succursale Centre-Ville, Montréal, Québec, Canada, H3C 3J7., INRS-Institut Armand-Frappier, 531 boul. des Prairies, Laval, Québec, Canada, H7V 1B7

^* To whom correspondence should be addressed. Email: france.daigle{at}umontreal.

	Abstract

Salmonella serovars contain a wide variety of putative fimbrial systems that may contribute to colonization of specific niches. Salmonella enterica serovar Typhi is the etiologic agent of typhoid fever and is a pathogen specific to humans. In a previous study, we identified a gene, STY3920 (stgC), encoding the predicted usher of the stg fimbrial operon, that was expressed by Typhi during infection of human macrophages. The stg genes are located in the glmS-pstS intergenic region in Typhi and certain E. coli, but are absent in other Salmonella enterica serovars. We cloned the stg fimbrial operon into a nonfimbriated E. coli K-12 strain and into Salmonella enterica serovar Typhimurium. We have demonstrated that the stg fimbrial operon contributed to increased adherence to human epithelial cells. Transcriptional fusion assays in serovar Typhi suggest that stg is preferentially expressed in minimal medium. The deletion of stg reduced adherence of Typhi to epithelial cells. However, the deletion of stg increased uptake of Typhi by human macrophages and its overexpression in Typhi and Typhimurium reduced phagocytosis by human macrophages. These strains survived inside macrophages as well as the wild-type parent. Although the stgC gene contains a premature stop codon that disrupts the expected ORF encoding the usher, and is therefore considered a pseudogene, our results show that the stg operon may encode for a functional fimbriae. Thus, this Typhi-specific fimbrial operon contributes to interaction with host cells, and further characterization will be important to understand the role of the stg fimbrial cluster in typhoid pathogenesis.