ArticleAllergy2008
The airway smooth muscle CCR3/CCL11 axis is inhibited by mast cells.
Article in Allergy, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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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.
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.
Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- CCR3 deficiency shifts adaptive to innate-driven immunity in asthma.The journal of allergy and clinical immunology. Global · 2025Article
- The proteolytic effect of mast cell tryptase to eotaxin-1/CCL11·eotaxin-2/CCL24 and eotaxin-3/CCL26 produced by conjunctival fibroblasts.Japanese journal of ophthalmology · 2019Article
- Schisandrin B down-regulated lncRNA BCYRN1 expression of airway smooth muscle cells by improving miR-150 expression to inhibit the proliferation and migration of ASMC in asthmatic rats.Cell proliferation · 2017Article
- Human Lung Mast Cell Products Regulate Airway Smooth Muscle CXCL10 Levels.Journal of allergy · 2014Article
- Anti-inflammatory dimethylfumarate: a potential new therapy for asthma?Mediators of inflammation · 2013Review
- Airway smooth muscle in asthma: just a target for bronchodilation?Clinics in chest medicine · 2012Review
- Article
- CC-chemokine CCL15 expression and possible implications for the pathogenesis of IgE-related severe asthma.Mediators of inflammation · 2012Review
- The pivotal role of airway smooth muscle in asthma pathophysiology.Journal of allergy · 2011Article
- Article
- Airway smooth muscle chemokine receptor expression and function in asthma.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundAirway smooth muscle hyperplasia is a feature of asthma, and increases with disease severity. CCR3-mediated recruitment of airway smooth muscle progenitors towards the airway smooth muscle bundle has been proposed as one possible mechanism involved in airway smooth muscle hyperplasia. Mast cells are microlocalized to the airway smooth muscle bundle and whether mast cells influence CCR3-mediated migration is uncertain.
methodsWe examined the expression of CCR3 by primary cultures of airway smooth muscle cells from asthmatics and nonasthmatics. CCR3 function was examined using intracellular calcium measurements, chemotaxis, wound healing, cell proliferation and survival assays. We investigated the recovery and function of both recombinant and airway smooth muscle-derived CCL11 (eotaxin) after co-culture with beta-tryptase and human lung mast cells.
resultsAirway smooth muscle expressed CCR3. Airway smooth muscle CCR3 activation by CCL11 mediated intracellular calcium elevation, concentration-dependent migration and wound healing, but had no effect on proliferation or survival. Co-culture with beta-tryptase or mast cells degraded recombinant and airway smooth muscle-derived CCL11, and beta-tryptase inhibited CCL11-mediated airway smooth muscle migration.
conclusionsCCL11 mediates airway smooth muscle migration. However co-culture with beta-tryptase or mast cells degraded recombinant and airway smooth muscle-derived CCL11 and inhibited CCL11-mediated airway smooth muscle migration. Therefore these findings cast doubt on the importance of the CCL11/CCR3 axis in the development of airway smooth muscle hyperplasia in asthma.
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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.