Evidence map›Paper›PMID 23682108›Full record

ArticleThe European respiratory journal2014

Interleukin-13 induces collagen type-1 expression through matrix metalloproteinase-2 and transforming growth factor-β1 in airway fibroblasts in asthma.

Rafael Firszt, Dave Francisco, Tony D Church, Joseph M Thomas, Jennifer L Ingram, Monica Kraft

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in The European respiratory journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03388359 (Role of Extracellular Matrix in the Development of Airway Remodeling in Asthma), which is not on this map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
4.2field-weighted citation impact, top 5% 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.

NCT03388359 naunknown statusnot on this mapstarted 2017, after this paper: background citation

Role of Extracellular Matrix in the Development of Airway Remodeling in Asthma

TypeinterventionalSponsorLithuanian University of Health SciencesRan2017 to 2020Enrolled60ConditionsAllergic Asthma, Airway Remodelling, Extracellular Matrix AlterationArmsBronchial challenge with allergen, Co-culture formation, Inhibition of Wnt and Smad signaling pathways, Extracellular matrix turnover and deposition assessment, Dermatophagoides pteronyssinus allergen
3 · Its place in the literature

Who cites it

66 citing papers in PubMed, 108 citations in OpenAlex.

  1. Trial
  2. Review
  3. Fibrotic chronic eosinophilic pneumonia: from inflammation to fibrosis and therapeutic implications.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Role of Mast Cells in Eosinophilic Gastrointestinal Diseases.Immunology and allergy clinics of North America · 2024
    Review
  16. Mast Cells in Aspirin-Exacerbated Respiratory Disease.Current allergy and asthma reports · 2024
    Review
  17. Review
  18. Review
  19. Review
  20. Review

6 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

Rafael FirsztDivision of Allergy, Immunology and Rheumatology, University of Utah, Salt Lake City, UT.
Dave Francisco
Tony D Church
Joseph M Thomas
Jennifer L Ingram
Monica Kraft
Duke University Hospital · USDuke Medical Center · USUniversity of Utah · US

Funding

MATRIX REGULATION OF FIBROPROLIFERATIVE LUNG DISEASEP50HL084917 · NHLBI · DUKE UNIVERSITY · PI WRIGHT, JO RAE · 2006 to 2010
$13.2M
NHLBI NIH HHS P50 HL084917PHS HHS NIH-NHLBI HL-05-009
6 · The paper itself

Abstract

Airway remodelling is a feature of asthma that contributes to loss of lung function. One of the central components of airway remodelling is subepithelial fibrosis. Interleukin (IL)-13 is a key T-helper 2 cytokine and is believed to be the central mediator of allergic asthma including remodelling, but the mechanism driving the latter has not been elucidated in human asthma. We hypothesised that IL-13 stimulates collagen type-1 production by the airway fibroblast in a matrix metalloproteinase (MMP)- and transforming growth factor (TGF)-β1-dependent manner in human asthma as compared to healthy controls. Fibroblasts were cultured from endobronchial biopsies in 14 subjects with mild asthma and 13 normal controls that underwent bronchoscopy. Airway fibroblasts were treated with various mediators including IL-13 and specific MMP-inhibitors. IL-13 significantly stimulated collagen type-1 production in asthma compared to normal controls. Inhibitors of MMP-2 significantly attenuated collagen production in asthma but had no effect in normal controls. IL-13 significantly increased total and active forms of TGF-β1, and this activation was blocked using an MMP-2 inhibitor. IL-13 activated endogenous MMP-2 in asthma patients as compared to normal controls. In an ex vivo model, IL-13 potentiates airway remodelling through a mechanism involving TGF-β1 and MMP-2. These effects provide insights into the mechanism involved in IL-13-directed airway remodelling in asthma.

Indexed as

Gene Expression RegulationActinsAdultAsthmabetaIG-H3 ProteinBiopsyBronchiCollagen Type IExtracellular Matrix ProteinsFemaleFibroblastsHumansInterleukin-13MaleMatrix Metalloproteinase 2Respiratory Function TestsActinsbetaIG-H3 ProteinCollagen Type IExtracellular Matrix ProteinsIL13 protein, humanInterleukin-13Matrix Metalloproteinase 2MMP2 protein, humanTransforming Growth Factor beta

Identifiers

PMID23682108
PMCPMC6747688
OpenAlexW2153642908

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.