Evidence map›Paper›PMID 27212082›Full record

ArticleThe Journal of allergy and clinical immunology2016

TGF-β1-induced PAI-1 contributes to a profibrotic network in patients with eosinophilic esophagitis.

Renee Rawson, Tom Yang, Robert O Newbury, Melissa Aquino, Ashmi Doshi, Braxton Bell, David H Broide, Ranjan Dohil, Richard Kurten, Seema S Aceves

Abstract read
In one paragraph

Article in The Journal of allergy and clinical immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
7.2field-weighted citation impact, top 3% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.

  1. Minimally invasive biomarker studies in eosinophilic esophagitis: A systematic review.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2018
    Pooled it
  2. Trial
  3. Eosinophilic gastrointestinal diseases.Nature reviews. Disease primers · 2026
    Review
  4. Review
  5. Article
  6. Immune functions of the esophagus.The Journal of allergy and clinical immunology · 2026
    Review
  7. Article
  8. Review
  9. The oesophagus as an immune organ.Nature reviews. Gastroenterology & hepatology · 2025
    Review
  10. Article
  11. Observational
  12. Development and dysfunction of structural cells in eosinophilic esophagitis.The Journal of allergy and clinical immunology · 2024
    Review
  13. Review
  14. Review
  15. Article
  16. ERBIN and phosphoglucomutase 3 deficiency.Current opinion in immunology · 2023
    Review
  17. Article
  18. Article
  19. Article
  20. 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

10 authors at 2 institutions in 1 country.

Renee RawsonDivision of Allergy and Immunology, Departments of Pediatrics and Medicine, University of California, San Diego, La Jolla, and Rady Children's Hospital, San Diego, Calif; Center for Infection, Immunity, and Inflammation, Departments of Pediatrics and Medicine, University of California, San Diego, La Jolla, and Rady Children's Hospital, San Diego, Calif.
Tom YangDivision of Allergy and Immunology, Departments of Pediatrics and Medicine, University of California, San Diego, La Jolla, and Rady Children's Hospital, San Diego, Calif; Center for Infection, Immunity, and Inflammation, Departments of Pediatrics and Medicine, University of California, San Diego, La Jolla, and Rady Children's Hospital, San Diego, Calif.
Robert O NewburyDepartment of Pediatric Pathology, Departments of Pediatrics and Medicine, University of California, San Diego, La Jolla, and Rady Children's Hospital, San Diego, Calif.
Melissa AquinoDivision of Allergy and Immunology, Departments of Pediatrics and Medicine, University of California, San Diego, La Jolla, and Rady Children's Hospital, San Diego, Calif.
Ashmi DoshiDivision of Allergy and Immunology, Departments of Pediatrics and Medicine, University of California, San Diego, La Jolla, and Rady Children's Hospital, San Diego, Calif; Center for Infection, Immunity, and Inflammation, Departments of Pediatrics and Medicine, University of California, San Diego, La Jolla, and Rady Children's Hospital, San Diego, Calif.
Braxton BellDivision of Allergy and Immunology, Departments of Pediatrics and Medicine, University of California, San Diego, La Jolla, and Rady Children's Hospital, San Diego, Calif; Center for Infection, Immunity, and Inflammation, Departments of Pediatrics and Medicine, University of California, San Diego, La Jolla, and Rady Children's Hospital, San Diego, Calif.
David H BroideDivision of Allergy and Immunology, Departments of Pediatrics and Medicine, University of California, San Diego, La Jolla, and Rady Children's Hospital, San Diego, Calif.
Ranjan DohilDivision of Pediatric Gastroenterology and Nutrition, Departments of Pediatrics and Medicine, University of California, San Diego, La Jolla, and Rady Children's Hospital, San Diego, Calif.
Richard KurtenDepartment of Physiology and Biophysics, University of Arkansas for Medical Sciences and Arkansas Children's Hospital Research Institute, Little Rock, Ark.
Seema S AcevesDivision of Allergy and Immunology, Departments of Pediatrics and Medicine, University of California, San Diego, La Jolla, and Rady Children's Hospital, San Diego, Calif; Center for Infection, Immunity, and Inflammation, Departments of Pediatrics and Medicine, University of California, San Diego, La Jolla, and Rady Children's Hospital, San Diego, Calif. Electronic address: saceves@ucsd.edu.
University of California San Diego · USArkansas Children's Hospital · US

Funding

UC San Diego Clinical and Translational Research InstituteUL1TR001442 · NCATS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FIRESTEIN, GARY S, HOGARTH, MICHAEL · 2015 to 2024
$88.3M
TRM and airway inflammation and remodelingU19AI070535 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROIDE, DAVID H · 2006 to 2025
$34.2M
San Diego Clinical and Translational Research InstituteUL1TR000100 · NCATS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FIRESTEIN, GARY S · 2012 to 2015
$19.7M
TRAINING (CAREER DEVELOPMENT) COMPONENTU54AI117804 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI GLENN T FURUTA, Marc E. Rothenberg · 2014 to 2026
$18.5M
Arkansas Center for Clinical and Translational ResearchUL1TR000039 · NCATS · UNIV OF ARKANSAS FOR MED SCIS · PI BECK, CORNELIA MARIE, JAMES, LAURA P · 2012 to 2014
$10.0M
Chromosome 17q, allergic inflammation, and remodelingR01AI107779 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROIDE, DAVID H · 2013 to 2024
$4.7M
Mechanisms of tissue damage leading to chronic allergic eosinophilic esophagitisR01AI092135 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ACEVES, SEEMA S · 2011 to 2020
$4.4M
Siglec-F and Resolution of Allergic InflammationR01AI072115 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROIDE, DAVID H · 2008 to 2012
$1.7M
Contribution of rigid matrix to allergic eosinophilic esophagitis pathogenesisR56AI092135 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ACEVES, SEEMA S · 2023 to 2023
$198k
NCATS NIH HHS UL1 TR000039NCATS NIH HHS UL1 TR000100NCATS NIH HHS UL1 TR001442NIAID NIH HHS R01 AI072115NIAID NIH HHS R01 AI092135NIAID NIH HHS R01 AI107779NIAID NIH HHS R56 AI092135NIAID NIH HHS U19 AI070535NIAID NIH HHS U54 AI117804
6 · The paper itself

Abstract

backgroundEosinophilic esophagitis (EoE) is an allergic disease of increasing worldwide incidence. Complications are due to tissue remodeling and involve TGF-β1-mediated fibrosis. Plasminogen activator inhibitor 1 (PAI-1/serpinE1) can be induced by TGF-β1, but its role in EoE is not known.

objectiveWe sought to understand the expression and role of PAI-1 in patients with EoE.

methodsWe used esophageal biopsy specimens and plasma samples from control subjects and patients with EoE, primary human esophageal epithelial cells, and fibroblasts from patients with EoE in immunohistochemistry, quantitative PCR, and immunoassay experiments to understand the induction of PAI-1 by TGF-β1, the relationship between PAI-1 and esophageal fibrosis, and the role of PAI-1 in fibrotic gene expression.

resultsPAI-1 expression was significantly increased in epithelial cells of biopsy specimens from patients with active EoE compared with that seen in biopsy specimens from patients with inactive EoE or control subjects (P < .001). Treatment of primary esophageal epithelial cells with recombinant TGF-β1 increased PAI-1 transcription, intracellular protein expression, and secretion. Esophageal PAI-1 expression correlated with basal zone hyperplasia, fibrosis, and markers of esophageal remodeling, including vimentin, TGF-β1, collagen I, fibronectin, and matrix metalloproteases, and plasma PAI-1 levels correlated with plasma TGF-β1 levels. PAI-1 inhibition significantly decreased baseline and TGF-β1-induced fibrotic gene expression.

conclusionsPAI-1 expression is significantly increased in the epithelium in patients with EoE and reflects fibrosis, and its inhibition decreases TGF-β1-induced gene expression. Epithelial PAI-1 might serve as a marker of EoE severity and form part of a TGF-β1-induced profibrotic network.

Indexed as

AdolescentChildChild, PreschoolEosinophilic EsophagitisEpithelial CellsEsophagusFemaleFibroblastsFibrosisHumansInfantMalePlasminogen Activator Inhibitor 1Transforming Growth Factor beta1Plasminogen Activator Inhibitor 1Transforming Growth Factor beta1EosinophilesophagitisfibrosisremodelingSerpinE1TGF-β1

Identifiers

PMID27212082
PMCPMC5014565
OpenAlexW2316469569

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Registered trials

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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.