Evidence map›Paper›PMID 23840906›Full record

ArticlePloS one2013

Enteric glia cells attenuate cytomix-induced intestinal epithelial barrier breakdown.

Gerald A Cheadle, Todd W Costantini, Nicole Lopez, Vishal Bansal, Brian P Eliceiri, Raul Coimbra

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.0field-weighted citation impact, top 7% 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

37 citing papers in PubMed, 95 citations in OpenAlex.

  1. Article
  2. Rodent Enteric Glia Culture.Methods in molecular biology (Clifton, N.J.) · 2026
    Article
  3. The Physiology of Enteric Glia.Annual review of physiology · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. A Mini Review ofNanomaterials (Basel, Switzerland) · 2023
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Enteric Glial Cells in Immunological Disorders of the Gut.Frontiers in cellular neuroscience · 2022
    Review
  19. Review
  20. A Novel Role of AFrontiers in pharmacology · 2021
    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

6 authors at 2 institutions in 1 country.

Gerald A CheadleDivision of Trauma, Surgical Critical Care, and Burns, Department of Surgery, University of California San Diego Health Sciences, San Diego, California, United States of America.
Todd W Costantini
Nicole Lopez
Vishal Bansal
Brian P Eliceiri
Raul Coimbra
University of California, San Diego · USUC San Diego Health System · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIntestinal barrier failure may lead to systemic inflammation and distant organ injury in patients following severe injury. Enteric glia cells (EGCs) have been shown to play an important role in maintaining gut barrier integrity through secretion of S-Nitrosoglutathione (GSNO). We have recently shown than Vagal Nerve Stimulation (VNS) increases EGC activation, which was associated with improved gut barrier integrity. Thus, we sought to further study the mechanism by which EGCs prevent intestinal barrier breakdown utilizing an in vitro model. We postulated that EGCs, through the secretion of GSNO, would improve intestinal barrier function through improved expression and localization of intestinal tight junction proteins.

methodsEpithelial cells were co-cultured with EGCs or incubated with GSNO and exposed to Cytomix (TNF-α, INF-γ, IL-1β) for 24 hours. Barrier function was assessed by permeability to 4kDa FITC-Dextran. Changes in tight junction proteins ZO-1, occludin, and phospho-MLC (P-MLC) were assessed by immunohistochemistry and immunoblot. KEY

resultsCo-culture of Cytomix-stimulated epithelial monolayers with EGCs prevented increases in permeability and improved expression and localization of occludin, ZO-1, and P-MLC. Further, treatment of epithelial monolayers with GSNO also prevented Cytomix-induced increases in permeability and exhibited a similar improvement in expression and localization of occludin, ZO-1, and P-MLC. CONCLUSIONS & INFERENCES: The addition of EGCs, or their secreted mediator GSNO, prevents epithelial barrier failure after injury and improved expression of tight junction proteins. Thus, therapies that increase EGC activation, such as VNS, may be a novel strategy to limit barrier failure in patients following severe injury.

Indexed as

PermeabilityAnimalsCell LineCoculture TechniquesHumansInterferon-gammaInterleukin-1betaIntestinal MucosaNeurogliaS-NitrosoglutathioneTight JunctionsTumor Necrosis Factor-alphaZonula Occludens-1 ProteinInterferon-gammaInterleukin-1betaS-NitrosoglutathioneTumor Necrosis Factor-alphaZonula Occludens-1 Protein

Identifiers

PMID23840906
PMCPMC3698076
OpenAlexW2060544572

What OpenQuestion holds

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LicenceCC BY
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.