Evidence map›Paper›PMID 22014415›Full record

ArticleJournal of comparative pathology2012

Uropathogenic E. coli promote a paracellular urothelial barrier defect characterized by altered tight junction integrity, epithelial cell sloughing and cytokine release.

M W Wood, E B Breitschwerdt, S K Nordone, K E Linder, J L Gookin

Open access · greenAbstract read
In one paragraph

Article in Journal of comparative pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
0.8field-weighted citation impact, top 26% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 40 citations in OpenAlex.

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  16. Review
  17. Urine: Waste product or biologically active tissue?Neurourology and urodynamics · 2018
    Article
  18. Review
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

M W WoodDepartment of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC 27607, USA.
E B Breitschwerdt
S K Nordone
K E Linder
J L Gookin
North Carolina State University · US

Funding

Comparative Medicine and Translational Research Training ProgramT32OD011130 · OD · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI Lauren Virginia Schnabel · 2012 to 2026
$7.8M
Comparative Medicine and Translational Research Training ProgramT32RR024394 · NCRR · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI JONES, SAMUEL L · 2008 to 2011
$1.1M
NCRR NIH HHS T32 RR024394NIH HHS T32 OD011130
6 · The paper itself

Abstract

The urinary bladder is a common site of bacterial infection with a majority of cases attributed to uropathogenic Escherichia coli. Sequelae of urinary tract infections (UTIs) include the loss of urothelial barrier function and subsequent clinical morbidity secondary to the permeation of urine potassium, urea and ammonia into the subepithelium. To date there has been limited research describing the mechanism by which this urothelial permeability defect develops. The present study models acute uropathogenic E. coli infection in vitro using intact canine bladder mucosa mounted in Ussing chambers to determine whether infection induces primarily a transcellular or paracellular permeability defect. The Ussing chamber sustains tissue viability while physically separating submucosal and lumen influences, so this model is ideal for quantitative measurement of transepithelial electrical resistance (TER) to assess alterations of urothelial barrier function. Using this model, changes in both tissue ultrastructure and TER indicated that uropathogenic E. coli infection promotes a paracellular permeability defect associated with the failure of umbrella cell tight junction formation and umbrella cell sloughing. In addition, bacterial interaction with the urothelium promoted secretion of cytokines from the urinary bladder with bioactivity capable of modulating epithelial barrier function including tumour necrosis factor-α, interleukin (IL)-6 and IL-15. IL-15 secretion by the infected bladder mucosa is a novel finding and, because IL-15 plays key roles in reconstitution of tight junction function in damaged intestine, this study points to a potential role for IL-15 in UTI-induced urothelial injury.

Indexed as

AnimalsCell Membrane PermeabilityCytokinesDiffusion Chambers, CultureDogsElectric ConductivityEpithelial CellsTight JunctionsTissue Culture TechniquesUrinary BladderUropathogenic Escherichia coliUrotheliumCytokines

Identifiers

PMID22014415
PMCPMC3695823
OpenAlexW2068688764

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.