Intracellular Uropathogenic . Exploits Host Rab35 for Iron Acquisition and Survival within Urinary Bladder Cells
Urinary tract infections (UTIs) are common and costly infectious diseases, affecting half of all women. Many women suffer from recurrent UTIs, for which no effective therapy currently exists. Intracellular persistence within bladder epithelial cells (BEC) by uropathogenic E. coli (UPEC) contributes to recurrent UTI in mouse models of infection. In the current study, we specifically asked whether and how UPEC co-opt any of the host proteins regulating vesicular trafficking for intracellular infection. Our study demonstrates a novel mechanism by which UPEC exploit a host endocytic recycling pathway protein (Rab35) to acquire the critical nutrient iron and to prevent lysosomal degradation, thereby promoting intracellular survival within BEC. The results of this study may highlight new avenues for therapeutic intervention in recurrent UTI. In addition, knowledge gained from this study can also be extended to understand the general principles by which other intracellular bacterial pathogens acquire essential nutrients, leading to additional strategies to combat these infectious diseases.
Vyšlo v časopise:
Intracellular Uropathogenic . Exploits Host Rab35 for Iron Acquisition and Survival within Urinary Bladder Cells. PLoS Pathog 11(8): e32767. doi:10.1371/journal.ppat.1005083
Kategorie:
Research Article
prolekare.web.journal.doi_sk:
https://doi.org/10.1371/journal.ppat.1005083
Souhrn
Urinary tract infections (UTIs) are common and costly infectious diseases, affecting half of all women. Many women suffer from recurrent UTIs, for which no effective therapy currently exists. Intracellular persistence within bladder epithelial cells (BEC) by uropathogenic E. coli (UPEC) contributes to recurrent UTI in mouse models of infection. In the current study, we specifically asked whether and how UPEC co-opt any of the host proteins regulating vesicular trafficking for intracellular infection. Our study demonstrates a novel mechanism by which UPEC exploit a host endocytic recycling pathway protein (Rab35) to acquire the critical nutrient iron and to prevent lysosomal degradation, thereby promoting intracellular survival within BEC. The results of this study may highlight new avenues for therapeutic intervention in recurrent UTI. In addition, knowledge gained from this study can also be extended to understand the general principles by which other intracellular bacterial pathogens acquire essential nutrients, leading to additional strategies to combat these infectious diseases.
Zdroje
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