Subversion of host innate immunity by uropathogenic escherichia coli

Patrick D. Olson, David A. Hunstad

Research output: Contribution to journalReview articlepeer-review

31 Scopus citations

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.

Original languageEnglish
Pages (from-to)1-10
Number of pages10
JournalPathogens
Volume5
Issue number1
DOIs
StatePublished - Jan 4 2016

Keywords

  • Cystitis
  • Effectors
  • Filamentation
  • Immune evasion
  • Intracellular bacterial communities
  • Neutrophils
  • Urinary tract infection

Fingerprint

Dive into the research topics of 'Subversion of host innate immunity by uropathogenic escherichia coli'. Together they form a unique fingerprint.

Cite this