Evidence map›Paper›PMID 25683166›Full record

ArticleAllergy2015

IL-33 drives airway hyper-responsiveness through IL-13-mediated mast cell: airway smooth muscle crosstalk.

D Kaur, E Gomez, C Doe, R Berair, L Woodman, R Saunders, F Hollins, F R Rose, Y Amrani, R May and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Allergy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed
6.5field-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

92 citing papers in PubMed, 161 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Cutaneous Wound Healing and the Effects of Cannabidiol.International journal of molecular sciences · 2024
    Review
  20. Article

32 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

14 authors at 4 institutions in 2 countries.

D KaurInstitute for Lung Health, Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, UK.
E Gomez
C Doe
R Berair
L Woodman
R Saunders
F Hollins
F R Rose
Y Amrani
R May
J Kearley
A Humbles
E S Cohen
C E Brightling
University of Leicester · GBAimmune Therapeutics (United Kingdom) · GBAltimmune (United States) · USUniversity of Nottingham · GB

Funding

National Centre for the Replacement, Refinement and Reduction of Animals in Research G1001804/1
6 · The paper itself

Abstract

backgroundMast cell localization within the airway smooth muscle (ASM)-bundle plays an important role in the development of airway hyper-responsiveness (AHR). Genomewide association studies implicate the 'alarmin' IL-33 in asthma, but its role in mast cell-ASM interactions is unknown.

objectivesWe examined the expression and functional role of IL-33 in bronchial biopsies of patients with and without asthma, ex vivo ASM, mast cells, cocultured cells and in a mouse model system.

methodsIL-33 protein expression was assessed in human bronchial tissue from 9 healthy controls, and 18 mild-to-moderate and 12 severe asthmatic patients by immunohistochemistry. IL-33 and ST2 mRNA and protein expression in human-derived ASM, epithelial and mast cells were assessed by qPCR, immunofluorescence and/or flow cytometry and ELISA. Functional assays were used to assess calcium signalling, wound repair, proliferation, apoptosis and contraction. AHR and inflammation were assessed in a mouse model.

resultsBronchial epithelium and ASM expressed IL-33 with the latter in asthma correlating with AHR. ASM and mast cells expressed intracellular IL-33 and ST2. IL-33 stimulated mast cell IL-13 and histamine secretion independent of FcεR1 cross-linking and directly promoted ASM wound repair. Coculture of mast cells with ASM activated by IL-33 increased agonist-induced ASM contraction, and in vivo IL-33 induced AHR in a mouse cytokine installation model; both effects were IL-13 dependent.

conclusionIL-33 directly promotes mast cell activation and ASM wound repair but indirectly promotes ASM contraction via upregulation of mast cell-derived IL-13. This suggests that IL-33 may present an important target to modulate mast cell-ASM crosstalk in asthma.

Indexed as

AdultAnimalsAsthmaBronchial HyperreactivityEnzyme-Linked Immunosorbent AssayFlow CytometryFluorescent Antibody TechniqueHumansImmunohistochemistryInterleukin-13Interleukin-33Mast CellsMiceMice, Inbred BALB CMice, Inbred C57BLMiddle AgedInterleukin-13Interleukin-33ASMIL-33mast cells

Identifiers

PMID25683166
PMCPMC4418379
OpenAlexW2044798842

What OpenQuestion holds

Textmetadata
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.