Study on the Promotion of Bacterial Biofilm Formation by a Salmonella Conjugative Plasmid and the Underlying Mechanism

To investigate the effect of the pR(ST98) plasmid, originally isolated from Salmonella enterica serovar Typhi (S. Typhi), on biofilm (BF) formation, we carried out in vitro experiments using S. Typhi, Salmonella enterica serovar Typhimurium (S. Typhimurium) and Escherichia coli (E. coli). We further explored the effects of pR(ST98) in vivo by establishing two animal models, a tumor-bearing mouse model and a mouse urethral catheter model. Moreover, we examined the relationship between the quorum-sensing (QS) system and pR(ST98)-mediated BF formation. These studies showed that pR(ST98) enhanced BF formation in different bacteria in vitro. In both animal models, pR(ST98) promoted BF formation and caused more severe pathological changes. It was previously reported that Salmonella senses exogenous N-acylhomoserine lactones (AHLs) through the regulatory protein SdiA and regulates the expression of genes including the virulence gene rck, which is located on the virulence plasmid of some serotypes of Salmonella. In this study, we confirmed the locus of the rck gene on pR(ST98) and found that AHLs increased rck expression in pR(ST98)-carrying strains, thereby enhancing bacterial adherence, serum resistance and bacterial BF formation. In conclusion, the Salmonella conjugative plasmid pR(ST98) promotes bacterial BF formation both in vitro and in vivo, and the mechanism may relate to the AHL-SdiA-Rck signaling pathway.