Evidence map›Paper›PMID 23180361›Full record

ArticleJournal of clinical immunology2013

Eosinophils induce airway smooth muscle cell proliferation.

Rabih Halwani, Alejandro Vazquez-Tello, Yuki Sumi, Mary Angeline Pureza, Ahmed Bahammam, Hamdan Al-Jahdali, Abdelillah Soussi-Gounni, Bassam Mahboub, Saleh Al-Muhsen, Qutayba Hamid

Abstract read
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In one paragraph

Article in Journal of clinical immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

31 citing papers in PubMed, 55 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Review
  5. Dog allergen-induced asthma in mice: a relevant model of T2Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  6. Review
  7. Type 2 immunity in allergic diseases.Cellular & molecular immunology · 2025
    Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Ameliorative Effect of Imperatorin onMolecules (Basel, Switzerland) · 2022
    Article
  18. Article
  19. αJournal of personalized medicine · 2021
    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 5 institutions in 3 countries.

Rabih HalwaniAsthma Research Chair and Prince Naif Center for Immunology Research, College of Medicine, King Saud University, Riyadh, Saudi Arabia.
Alejandro Vazquez-Tello
Yuki Sumi
Mary Angeline Pureza
Ahmed Bahammam
Hamdan Al-Jahdali
Abdelillah Soussi-Gounni
Bassam Mahboub
Saleh Al-Muhsen
Qutayba Hamid
King Saud University · SAChristie (Canada) · CAMcGill University · CAUniversity of Manitoba · CAUniversity of Sharjah · AE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Asthma is characterized by eosinophilic airway inflammation and remodeling of the airway wall. Features of airway remodeling include increased airway smooth muscle (ASM) mass. However, little is known about the interaction between inflammatory eosinophils and ASM cells. In this study, we investigated the effect of eosinophils on ASM cell proliferation. Eosinophils were isolated from peripheral blood of mild asthmatics and non-asthmatic subjects and co-cultured with human primary ASM cells. ASM proliferation was estimated using Ki-67 expression assay. The expression of extracellular matrix (ECM) mRNA in ASM cells was measured using quantitative real-time PCR. The role of eosinophil derived Cysteinyl Leukotrienes (CysLTs) in enhancing ASM proliferation was estimated by measuring the release of leukotrienes from eosinophils upon their direct contact with ASM cells using ELISA. This role was confirmed either by blocking eosinophil-ASM contact or co-culturing them in the presence of leukotrienes antagonist. ASM cells co-cultured with eosinophils, isolated from asthmatics, but not non-asthmatics, had a significantly higher rate of proliferation compared to controls. This increase in ASM proliferation was independent of their release of ECM proteins but dependent upon eosinophils release of CysLTs. Eosinophil-ASM cell to cell contact was required for CysLTs release. Preventing eosinophil contact with ASM cells using anti-adhesion molecules antibodies, or blocking the activity of eosinophil derived CysLTs using montelukast inhibited ASM proliferation. Our results indicated that eosinophils contribute to airway remodeling during asthma by enhancing ASM cell proliferation and hence increasing ASM mass. Direct contact of eosinophils with ASM cells triggers their release of CysLTs which enhance ASM proliferation. Eosinophils, and their binding to ASM cells, constitute a potential therapeutic target to interfere with the series of biological events leading to airway remodeling and Asthma.

Indexed as

AdultAirway RemodelingAsthmaCell CommunicationCell ProliferationCoculture TechniquesEosinophilsFemaleHumansLeukocyte CountLeukotrienesMaleMyocytes, Smooth MuscleRespiratory SystemSignal TransductionLeukotrienes

Identifiers

PMID23180361
OpenAlexW2019638372

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.