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Permanent link (DOI): https://doi.org/10.7939/R3R20S93C

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Small intestine early innate immunity response during intestinal colonization by Escherichia coli depends on its extra-intestinal virulence status Open Access

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Author or creator
Tourret, Jérôme
Willing, Benjamin P.
Croxen, Matthew A.
Dufour, Nicolas
Dion, Sara
Wachtel, Sarah
Denamur, Erick
Finlay, B. Brett
Additional contributors
Subject/Keyword
Bacterial Pathogens
Cytokines
Gastrointestinal Tract
Virulence Factors
Inflammation
Ileum
Enterobacteriaceae
Escherichia coli Infections
Type of item
Journal Article (Published)
Language
English
Place
Time
Description
Uropathogenic Escherichia coli (UPEC) strains live as commensals in the digestive tract of the host, but they can also initiate urinary tract infections. The aim of this work was to determine how a host detects the presence of a new UPEC strain in the digestive tract. Mice were orally challenged with UPEC strains 536 and CFT073, non-pathogenic strain K12 MG1655, and ΔPAI-536, an isogenic mutant of strain 536 lacking all 7 pathogenicity islands whose virulence is drastically attenuated. Intestinal colonization was measured, and cytokine expression was determined in various organs recovered from mice after oral challenge. UPEC strain 536 efficiently colonized the mouse digestive tract, and prior Enterobacteriaceae colonization was found to impact strain 536 colonization efficiency. An innate immune response, detected as the production of TNFα, IL-6 and IL-10 cytokines, was activated in the ileum 48 hours after oral challenge with strain 536, and returned to baseline within 8 days, without a drop in fecal pathogen load. Although inflammation was detected in the ileum, histology was normal at the time of cytokine peak. Comparison of cytokine secretion 48h after oral gavage with E. coli strain 536, CFT073, MG1655 or ΔPAI-536 showed that inflammation was more pronounced with UPECs than with non-pathogenic or attenuated strains. Pathogenicity islands also seemed to be involved in host detection, as IL-6 intestinal secretion was increased after administration of E. coli strain 536, but not after administration of ΔPAI-536. In conclusion, UPEC colonization of the mouse digestive tract activates acute phase inflammatory cytokine secretion but does not trigger any pathological changes, illustrating the opportunistic nature of UPECs. This digestive tract colonization model will be useful for studying the factors controlling the switch from commensalism to pathogenicity.
Date created
2016
DOI
doi:10.7939/R3R20S93C
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Attribution 4.0 International
Citation for previous publication
Tourret, J., Willing, B. P., Croxen, M. A., Dufour, N., Dion, S., Wachtel, S., Denamur, E., & Finlay, B. B. (2016). Small intestine early innate immunity response during intestinal colonization by Escherichia coli depends on its extra-intestinal virulence status. PLoS ONE, 11(4), e0153034 [14 pages].  http://dx.doi.org/10.1371/journal.pone.0153034

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File title: Small Intestine Early Innate Immunity Response during Intestinal Colonization by Escherichia coli Depends on Its Extra-Intestinal Virulence Status
File author: Jérôme Tourret, Benjamin P. Willing, Matthew A. Croxen, Nicolas Dufour, Sara Dion, Sarah Wachtel, Erick Denamur, B. Brett Finlay
File author: Jrme Tourret, Benjamin P. Willing, Matthew A. Croxen, Nicolas Dufour, Sara Dion, Sarah Wachtel, Erick Denamur, B. Brett Finlay
Page count: 14
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