Filamentation byEscherichia colisubverts innate defenses during urinary tract infection
| العنوان: | Filamentation byEscherichia colisubverts innate defenses during urinary tract infection |
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| المؤلفون: | Patrick C. Seed, Scott J. Hultgren, Sheryl S. Justice, David A. Hunstad |
| المصدر: | Proceedings of the National Academy of Sciences. 103:19884-19889 |
| بيانات النشر: | Proceedings of the National Academy of Sciences, 2006. |
| سنة النشر: | 2006 |
| مصطلحات موضوعية: | Multidisciplinary, Innate immune system, Virulence, Cell division, Escherichia coli Proteins, Gene Expression Regulation, Bacterial, Biological Sciences, Biology, medicine.disease_cause, Phenotype, Microbiology, Toll-Like Receptor 4, Mice, Urinary Tract Infections, Escherichia coli, medicine, TLR4, Animals, Humans, SOS response, skin and connective tissue diseases, Intracellular |
| الوصف: | To establish disease, an infecting organism must overcome a vast array of host defenses. During cystitis, uropathogenicEscherichia coli(UPEC) subvert innate defenses by invading superficial umbrella cells and rapidly increasing in numbers to form intracellular bacterial communities (IBCs). In the late stages of the IBC pathway, filamentous and bacillary UPEC detach from the biofilm-like IBC, fluxing out of this safe haven to colonize the surrounding epithelium and initiate subsequent generations of IBCs, and eventually they establish a quiescent intracellular reservoir. Filamentous UPEC are not observed during acute infection in mice lacking functional Toll-like receptor 4 (TLR4), suggesting that the filamentous phenotype arises in response to host innate immunity. We investigated SulA, a cell division inhibitor associated with the SOS response, to gain insight into the role of filamentous UPEC in pathogenesis. A transcriptional reporter from PsulArevealed spatial and temporal differences in expression within IBCs, and it was active in the majority of filamentous UPEC. Although UTI89 and UTI89 ΔsulAboth formed first-generation IBCs equally well, UTI89 ΔsulAwas sharply attenuated in formation of second-generation IBCs and establishment of the quiescent intracellular reservoir. The virulence of UTI89 ΔsulAwas restored in TLR4-deficient mice, suggesting that filamentation facilitates the transition to additional rounds of IBC formation by subverting innate immune responses. These findings demonstrate that transient SulA-mediated inhibition of cell division is essential for UPEC virulence in the murine model of cystitis. |
| تدمد: | 1091-6490 0027-8424 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::93acd5c557f9c0440dda25c5f820c459Test https://doi.org/10.1073/pnas.0606329104Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....93acd5c557f9c0440dda25c5f820c459 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 10916490 00278424 |
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