Evidence map›Paper›PMID 27795363›Full record

ArticleInfection and immunity2017

Tricellular Tight Junction Protein Tricellulin Is Targeted by the Enteropathogenic Escherichia coli Effector EspG1, Leading to Epithelial Barrier Disruption.

Vijay Morampudi, Franziska A Graef, Martin Stahl, Udit Dalwadi, Victoria S Conlin, Tina Huang, Bruce A Vallance, Hong B Yu, Kevan Jacobson

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
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  4. Review
  5. Article
  6. Review
  7. Immune-Mediated Aggravation of theInternational journal of molecular sciences · 2021
    Article
  8. Observational
  9. Article
  10. Review
  11. Review
  12. Article
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

9 authors at 2 institutions in 1 country.

Vijay MorampudiChild and Family Research Institute, BC Children's Hospital, Vancouver, British Columbia, Canada.
Franziska A GraefChild and Family Research Institute, BC Children's Hospital, Vancouver, British Columbia, Canada.
Martin StahlChild and Family Research Institute, BC Children's Hospital, Vancouver, British Columbia, Canada.
Udit DalwadiChild and Family Research Institute, BC Children's Hospital, Vancouver, British Columbia, Canada.
Victoria S ConlinChild and Family Research Institute, BC Children's Hospital, Vancouver, British Columbia, Canada.
Tina HuangChild and Family Research Institute, BC Children's Hospital, Vancouver, British Columbia, Canada.
Bruce A VallanceChild and Family Research Institute, BC Children's Hospital, Vancouver, British Columbia, Canada.
Hong B YuChild and Family Research Institute, BC Children's Hospital, Vancouver, British Columbia, Canada.
Kevan JacobsonChild and Family Research Institute, BC Children's Hospital, Vancouver, British Columbia, Canada kjacobson@cw.bc.ca.
Child and Family Research Institute · CABC Children's Hospital · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Enteropathogenic Escherichia coli (EPEC)-induced diarrhea is often associated with disruption of intestinal epithelial tight junctions. Although studies have shown alterations in the expression and localization of bicellular tight junction proteins during EPEC infections, little is known about whether tricellular tight junction proteins (tTJs) are affected. Using Caco-2 cell monolayers, we investigated if EPEC is capable of targeting the tTJ protein tricellulin. Our results demonstrated that at 4 h postinfection, EPEC induced a significant reduction in tricellulin levels, accompanied by a significant loss of transepithelial resistance (TEER) and a corresponding increase in paracellular permeability. Conversely, cells overexpressing tricellulin were highly resistant to EPEC-induced barrier disruption. Confocal microscopy revealed the distribution of tricellulin into the plasma membrane of infected epithelial cells and confirmed the localization of EPEC aggregates in close proximity to tTJs. Moreover, infections with EPEC strains lacking genes encoding specific type III secreted effector proteins demonstrated a crucial role for the effector EspG1 in modulating tricellulin expression. Complementation studies suggest that the EspG-induced depletion of tricellulin is microtubule dependent. Overall, our results show that EPEC-induced epithelial barrier dysfunction is mediated in part by EspG1-induced microtubule-dependent depletion of tricellulin.

Indexed as

Caco-2 CellsCell Line, TumorDiarrheaEnteropathogenic Escherichia coliEpithelial CellsEscherichia coli InfectionsEscherichia coli ProteinsHumansMARVEL Domain Containing 2 ProteinMicrotubule-Associated ProteinsMicrotubulesPermeabilityTight JunctionsEscherichia coli ProteinsEspG1 protein, E coliMARVEL Domain Containing 2 ProteinMicrotubule-Associated Proteinsenteropathogenic Escherichia coliepithelial barrier functionEspGtight junctionstricellulintype III secretion systemvirulence

Identifiers

PMID27795363
PMCPMC5203647
OpenAlexW2533577972

What OpenQuestion holds

Textmetadata
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.