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RpoS Contributes to Phagocyte Oxidase-Mediated Stress Resistance during Urinary Tract Infection by Escherichia coli CFT073

Uropathogenic Escherichia coli (UPEC) is the most common causative agent of community-acquired urinary tract infection (UTI). In order to cause UTI, UPEC must endure stresses ranging from nutrient limitation to host immune components. RpoS (σ(S)), the general stress response sigma factor, directs ge...

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Autores principales: Hryckowian, Andrew J., Welch, Rodney A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: American Society of Microbiology 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3573659/
https://www.ncbi.nlm.nih.gov/pubmed/23404396
http://dx.doi.org/10.1128/mBio.00023-13
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author Hryckowian, Andrew J.
Welch, Rodney A.
author_facet Hryckowian, Andrew J.
Welch, Rodney A.
author_sort Hryckowian, Andrew J.
collection PubMed
description Uropathogenic Escherichia coli (UPEC) is the most common causative agent of community-acquired urinary tract infection (UTI). In order to cause UTI, UPEC must endure stresses ranging from nutrient limitation to host immune components. RpoS (σ(S)), the general stress response sigma factor, directs gene expression under a variety of inhibitory conditions. Our study of rpoS in UPEC strain CFT073 began after we discovered an rpoS-frameshift mutation in one of our laboratory stocks of “wild-type” CFT073. We demonstrate that an rpoS-deletion mutation in CFT073 leads to a colonization defect during UTI of CBA/J mice at 48 hours postinfection (hpi). There is no difference between the growth rates of CFT073 and CFT073 rpoS in urine. This indicates that rpoS is needed for replication and survival in the host rather than being needed to address limitations imposed by urine nutrients. Consistent with previous observations in E. coli K-12, CFT073 rpoS is more sensitive to oxidative stress than the wild type. We demonstrate that peroxide levels are elevated in voided urine from CFT073-infected mice compared to urine from mock-infected mice, which supports the notion that oxidative stress is generated by the host in response to UPEC. In mice that lack phagocyte oxidase, the enzyme complex expressed by phagocytes that produces superoxide, the competitive defect of CFT073 rpoS in bladder colonization is lost. These results demonstrate that σ(S) is important for UPEC survival under conditions of phagocyte oxidase-generated stress during UTI. Though σ(S) affects the pathogenesis of other bacterial species, this is the first work that directly implicates σ(S) as important for UPEC pathogenesis.
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spelling pubmed-35736592013-02-19 RpoS Contributes to Phagocyte Oxidase-Mediated Stress Resistance during Urinary Tract Infection by Escherichia coli CFT073 Hryckowian, Andrew J. Welch, Rodney A. mBio Research Article Uropathogenic Escherichia coli (UPEC) is the most common causative agent of community-acquired urinary tract infection (UTI). In order to cause UTI, UPEC must endure stresses ranging from nutrient limitation to host immune components. RpoS (σ(S)), the general stress response sigma factor, directs gene expression under a variety of inhibitory conditions. Our study of rpoS in UPEC strain CFT073 began after we discovered an rpoS-frameshift mutation in one of our laboratory stocks of “wild-type” CFT073. We demonstrate that an rpoS-deletion mutation in CFT073 leads to a colonization defect during UTI of CBA/J mice at 48 hours postinfection (hpi). There is no difference between the growth rates of CFT073 and CFT073 rpoS in urine. This indicates that rpoS is needed for replication and survival in the host rather than being needed to address limitations imposed by urine nutrients. Consistent with previous observations in E. coli K-12, CFT073 rpoS is more sensitive to oxidative stress than the wild type. We demonstrate that peroxide levels are elevated in voided urine from CFT073-infected mice compared to urine from mock-infected mice, which supports the notion that oxidative stress is generated by the host in response to UPEC. In mice that lack phagocyte oxidase, the enzyme complex expressed by phagocytes that produces superoxide, the competitive defect of CFT073 rpoS in bladder colonization is lost. These results demonstrate that σ(S) is important for UPEC survival under conditions of phagocyte oxidase-generated stress during UTI. Though σ(S) affects the pathogenesis of other bacterial species, this is the first work that directly implicates σ(S) as important for UPEC pathogenesis. American Society of Microbiology 2013-02-12 /pmc/articles/PMC3573659/ /pubmed/23404396 http://dx.doi.org/10.1128/mBio.00023-13 Text en Copyright © 2013 Hryckowian and Welch. http://creativecommons.org/licenses/by-nc-sa/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-ShareAlike 3.0 Unported (http://creativecommons.org/licenses/by-nc-sa/3.0/) license , which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Hryckowian, Andrew J.
Welch, Rodney A.
RpoS Contributes to Phagocyte Oxidase-Mediated Stress Resistance during Urinary Tract Infection by Escherichia coli CFT073
title RpoS Contributes to Phagocyte Oxidase-Mediated Stress Resistance during Urinary Tract Infection by Escherichia coli CFT073
title_full RpoS Contributes to Phagocyte Oxidase-Mediated Stress Resistance during Urinary Tract Infection by Escherichia coli CFT073
title_fullStr RpoS Contributes to Phagocyte Oxidase-Mediated Stress Resistance during Urinary Tract Infection by Escherichia coli CFT073
title_full_unstemmed RpoS Contributes to Phagocyte Oxidase-Mediated Stress Resistance during Urinary Tract Infection by Escherichia coli CFT073
title_short RpoS Contributes to Phagocyte Oxidase-Mediated Stress Resistance during Urinary Tract Infection by Escherichia coli CFT073
title_sort rpos contributes to phagocyte oxidase-mediated stress resistance during urinary tract infection by escherichia coli cft073
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3573659/
https://www.ncbi.nlm.nih.gov/pubmed/23404396
http://dx.doi.org/10.1128/mBio.00023-13
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