Abstract
BackgroundUrinary tract infections (UTI) are among the most common and costly infections in both hospitalized and ambulatory patients. Uropathogenic E. coli (UPEC) represent the majority of UTI isolates and are a diverse group of bacteria that utilize a variety of virulence factors to establish infection of the genitourinary tract. The virulence factor cytotoxic necrotizing factor-1 (CNF1) is frequently expressed in clinical UPEC isolates. To date, there have been conflicting reports on the role of CNF1 in the pathogenesis of E. coli urinary tract infections.ResultsWe examined the importance of CNF1 in a murine ascending kidney infection/ pyelonephritis model by performing comparative studies between a clinical UPEC isolate strain and a CNF1-deletion mutant. We found no alterations in bacterial burden with the loss of CNF1, whereas loss of the virulence factor fimH decreased bacterial burdens. In addition, we found no evidence that CNF1 contributed to the recruitment of inflammatory infiltrates in the kidney or bladder in vivo.ConclusionsWhile further examination of CNF-1 may reveal a role in UTI pathogenesis, our data casts doubt on the role of CNF-1 in the pathogenesis of UPEC UTI. As with other infections, different models and approaches are needed to elucidate the contribution of CNF1 to E. coli UTI.
Highlights
Urinary tract infections (UTI) are among the most common and costly infections in both hospitalized and ambulatory patients
Effect of cnf1 deletion on E. coli infection in the murine urinary tract The E. coli virulence factor cytotoxic necrotizing factor-1 (CNF1) has been previously implicated in the pathogenesis of Uropathogenic E. coli (UPEC) bladder infection but its potential role in kidney infection remains unknown [28]
To examine the role of CNF1 in the pathogenesis of pyelonephritis, we used a murine model of ascending pyelonephritis following transurethral instillation of E. coli [35, 36]
Summary
Urinary tract infections (UTI) are among the most common and costly infections in both hospitalized and ambulatory patients. Uropathogenic E. coli (UPEC) represent the majority of UTI isolates and are a diverse group of bacteria that utilize a variety of virulence factors to establish infection of the genitourinary tract. There have been conflicting reports on the role of CNF1 in the pathogenesis of E. coli urinary tract infections. Between 10 and 20% of United States women report at least one UTI and over 1 million hospitalized patients develop catheter-associated UTI annually [2, 3]. Most episodes of cystitis respond to Uropathogenic E. coli (UPEC) are the most common cause of UTI and are isolated in over 70% of cystitis or UTI-related bacteremia cultures [9, 10]. P fimbriae, or pyelonephritis-associated pili, are preferentially expressed in pyelonephritis isolates of UPEC and bind to glycosphingolipids present on renal epithelial cells [16, 17]
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