Abstract
Urinary tract infections primarily caused by uropathogenic strains of Escherichia coli (E. coli) remain a significant public health problem in both developed and developing countries. An important virulence determinant in uropathogenesis is biofilm formation which requires expression of fimbriae, flagella, and other surface components such as lipopolysaccharides. In this study, we explored the regulation of uvrY and csrA genes in biofilm formation, motility and virulence determinants in uropathogenic E. coli. We found that mutation in uvrY suppressed biofilm formation on abiotic surfaces such as polyvinyl chloride, polystyrene and glass, and complementation of uvrY in the mutant restored the biofilm phenotype. We further evaluated the role of uvrY gene in expression of type 1 fimbriae, an important adhesin that facilitates adhesion to various abiotic surfaces. We found that phase variation of type 1 fimbriae between fimbriated and afimbriated mode was modulated by uvrY at its transcriptional level. Deletion mutant of uvrY lowered expression of fimbrial recombinase genes, such as fimB, fimE, and fimA, a gene encoding major fimbrial subunit. Furthermore, transcription of virulence specific genes such as papA, hlyB and galU was also reduced in the deletion mutant. Swarming motility and expression of flhD and flhC was also diminished in the mutant. Taken together, our findings unravel a possible mechanism in which uvrY facilitates biofilm formation, persistence and virulence of uropathogenic E. coli.
Highlights
Uropathogenic Escherichia coli (UPEC) causes urinary tract infections, and septicemia in humans and animals [1,2]
Our results showed that deletion of uvrY in CFT073 abolished biofilm production on abiotic surface such as polystyrene, PVC or borosilicate glass (Fig. 1A, B & C, lane 2), as compared to that of the wild-type (Fig. 1A, B & C, lane 1)
Loss of uvrY diminished attachment to glass at all-time tested on the glass surface (Fig. 1C, lane 2). These results suggest that the uvrY gene product significantly facilitates the biofilm development, whereas the over-expression of csrA leads to inhibition of biofilm formation in CFT073 strain
Summary
Uropathogenic Escherichia coli (UPEC) causes urinary tract infections (cystitis, pyelonephritis), and septicemia in humans and animals [1,2]. In UPEC, the initial process of attachment is mediated by several adhesins, of which, type 1 and pap fimbriae play a critical role in colonization in urinary bladder and kidneys respectively. The fimbriae exhibit phase variation by inversion of a 314-bp DNA element (fim switch), which harbors the promoter for several structural proteins [7,8]. This allows (‘‘on’’ orientation) or prevents (‘‘off’’ orientation) transcription of the structural genes in E. coli
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