Urinary tract infections caused by Pseudomonas aeruginosa: a minireview

Urinary tract infections [UTIs] are a serious health problem affecting millions of people each year. Infections of the urinary tract are the second most common type of infection in the body. Catheterization of the urinary tract is the most common factor, which predisposes the host to these infections. Catheter-associated UTI [CAUTI] is responsible for 40% of nosocomial infections, making it the most common cause of nosocomial infection. CAUTI accounts for more than 1 million cases in hospitals and nursing homes annually and often involve uropathogens other than Escherichia coli. While the epidemiology and pathogenic mechanisms of uropathogenic Escherichia coli have been extensively studied, little is known about the pathogenesis of UTIs caused by other organisms like Pseudomonas aeruginosa. Scanty available information regarding pathogenesis of UTIs caused by P. aeruginosa is an important bottleneck in developing effective preventive approaches. The aim of this review is to summarize some of the advances made in the field of P. aeruginosa induced UTIs and draws attention of the workers that more basic research at the level of pathogenesis is needed so that novel strategies can be designed

Evaluation of interleukin-10 production in pseudomonas aeruginosa induced acute pyelonephritis

Pseudomonas aeruginosa is an opportunistic pathogen of immunocompromised hosts. This pathogen has a tendency to form biofilms on the surface of indwelling catheters leading to acute and chronic urinary tract infections that result in significant morbidity and mortality. In the present study, kinetics of interleukin-10 [IL-10] production in mouse renal tissue was studied employing experimental mouse model of acute pyelonephritis induced with planktonic and biofilm cells of P. aeruginosa. IL-10 production was found to be significantly lower in biofilm cell instilled mice compared to planktonic cell infected animals, which corroborated with higher bacterial load and tissue damage. The data suggests that downregulation of IL-10 production may be novel strategy employed by biofilm cells to cause tissue damage and hence bacterial persistence. The results of the present study may open up avenues of research that will ultimately provide the foundation for the development of preventative measures and therapeutic strategies to successfully treat P. aeruginosa biofilm infections based on the administration of anti-inflammatory agents