Evidence map›Paper›PMID 16601090›Full record

ArticleThorax2006

Mast cell migration to Th2 stimulated airway smooth muscle from asthmatics.

A Sutcliffe, D Kaur, S Page, L Woodman, C L Armour, M Baraket, P Bradding, J M Hughes, C E Brightling

Open access · bronzeAbstract readMulticenter Study
In one paragraph

Article in Thorax, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.8field-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

23 citing papers in PubMed, 56 citations in OpenAlex.

  1. Allergen Immunotherapy for the Prevention and Treatment of Asthma.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2025
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Asthma and COPD - The C/EBP Connection.The open respiratory medicine journal · 2012
    Article
  10. Article
  11. Chronic inflammation and asthma.Mutation research · 2010
    Review
  12. Airway smooth muscle proliferation and survival is not modulated by mast cells.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2010
    Article
  13. Interleukin-13: prospects for new treatments.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2010
    Review
  14. Article
  15. Review
  16. Article
  17. Structural aspects of airway remodeling in asthma.Current allergy and asthma reports · 2008
    Review
  18. Article
  19. Tyrosine sulfation is prevalent in human chemokine receptors important in lung disease.American journal of respiratory cell and molecular biology · 2008
    Article
  20. Asthma from a pharmacogenomic point of view.British journal of pharmacology · 2008
    Review
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

9 authors at 1 institution in 1 country.

A SutcliffeInstitute for Lung Health, Department of Infection, University of Leicester, Leicester, UK.
D Kaur
S Page
L Woodman
C L Armour
M Baraket
P Bradding
J M Hughes
C E Brightling
NIHR Leicester Biomedical Research Centre · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMast cell microlocalisation within the airway smooth muscle (ASM) bundle is an important determinant of the asthmatic phenotype. We hypothesised that mast cells migrate towards ASM in response to ASM derived chemokines.

methodsPrimary ASM cultures from subjects with and without asthma were stimulated with interleukin (IL)-1beta, IL-4, and IL-13 alone and in combination. Mast cell chemotaxis towards these ASM supernatants was investigated, and the chemotaxins mediating migration by using specific blocking antibodies for stem cell factor (SCF) and the chemokine receptors CCR3, CXCR1, 3 and 4 as well as the Gi inhibitor pertussis toxin and the tyrosine kinase inhibitor genistein were defined. The concentrations of CCL11, CXCL8, CXCL10, TGF-beta, and SCF in the supernatants were measured and the effect of non-asthmatic ASM supernatants on the mast cell chemotactic activity of asthmatic ASM was examined.

resultsHuman lung mast cells and HMC-1 cells migrated towards Th2 stimulated ASM from asthmatics but not non-asthmatics. Mast cell migration was mediated through the combined activation of CCR3 and CXCR1. CCL11 and CXCL8 expression by ASM increased markedly after stimulation, but was similar in those with and without asthma. ASM supernatants from non-asthmatics inhibited mast cell migration towards the asthmatic ASM supernatant.

conclusionTh2 stimulated ASM from asthmatics is chemotactic for mast cells. Non-asthmatic ASM releases a mediator or mediators that inhibit mast cell migration towards stimulated asthmatic ASM. Specifically targeting mast cell migration into the ASM bundle may provide a novel treatment for asthma.

Indexed as

AsthmaBronchiCell LineChemokinesChemotaxisGenisteinHumansInterleukinsMast CellsMuscle, SmoothPertussis ToxinReceptors, ChemokineStem Cell FactorTh2 CellsTransforming Growth Factor betaChemokinesGenisteinInterleukinsPertussis ToxinReceptors, ChemokineStem Cell FactorTransforming Growth Factor beta

Identifiers

PMID16601090
PMCPMC2104682
OpenAlexW2137613354

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.