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Pathogens 2016, 5(1), 2; doi:10.3390/pathogens5010002

Subversion of Host Innate Immunity by Uropathogenic Escherichia coli

1
Medical Scientist Training Program, Washington University School of Medicine, 660 S. Euclid Ave., Campus Box 8208, St. Louis, MO 63110, USA
2
Departments of Pediatrics and Molecular Microbiology, Washington University School of Medicine, 660 S. Euclid Ave., Campus Box 8208, St. Louis, MO 63110, USA
*
Author to whom correspondence should be addressed.
Academic Editor: Catharina Svanborg
Received: 16 July 2015 / Revised: 3 August 2015 / Accepted: 29 December 2015 / Published: 4 January 2016
(This article belongs to the Special Issue Molecular Aspects of Urinary Tract Infection)
View Full-Text   |   Download PDF [626 KB, uploaded 4 January 2016]   |  

Abstract

Uropathogenic Escherichia coli (UPEC) cause the majority of community-onset urinary tract infections (UTI) and represent a major etiologic agent of healthcare-associated UTI. Introduction of UPEC into the mammalian urinary tract evokes a well-described inflammatory response, comprising pro-inflammatory cytokines and chemokines as well as cellular elements (neutrophils and macrophages). In human UTI, this inflammatory response contributes to symptomatology and provides means for diagnosis by standard clinical testing. Early in acute cystitis, as demonstrated in murine models, UPEC gains access to an intracellular niche that protects a population of replicating bacteria from arriving phagocytes. To ensure the establishment of this protected niche, UPEC employ multiple strategies to attenuate and delay the initiation of host inflammatory components, including epithelial secretion of chemoattractants. Recent work has also revealed novel mechanisms by which UPEC blunts neutrophil migration across infected uroepithelium. Taken together, these attributes distinguish UPEC from commensal and nonpathogenic E. coli strains. This review highlights the unique immune evasion and suppression strategies of this bacterial pathogen and offers directions for further study; molecular understanding of these mechanisms will inform the development of adjunctive, anti-virulence therapeutics for UTI. View Full-Text
Keywords: urinary tract infection; immune evasion; effectors; neutrophils; intracellular bacterial communities; filamentation; cystitis urinary tract infection; immune evasion; effectors; neutrophils; intracellular bacterial communities; filamentation; cystitis
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Olson, P.D.; Hunstad, D.A. Subversion of Host Innate Immunity by Uropathogenic Escherichia coli. Pathogens 2016, 5, 2.

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