ArticleAmerican journal of respiratory and critical care medicine2011
Mast cell phenotype, location, and activation in severe asthma. Data from the Severe Asthma Research Program.
Article in American journal of respiratory and critical care medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers, 2 of them syntheses that pooled it.
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.
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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.
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Who cites it
139 citing papers in PubMed, 2 syntheses or guidelines pooled it, 292 citations in OpenAlex.
- Discerning asthma endotypes through comorbidity mapping.Nature communications · 2022Pooled it
- Efficacy and Safety of Prostaglandin D2 Receptor 2 Antagonism with Fevipiprant for Patients with Asthma: a Systematic Review and Meta-analysis of Randomized Controlled Trials.Current allergy and asthma reports · 2021Pooled it
- Circulating mast cell progenitors correlate with reduced lung function in allergic asthma.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2019Trial
- Efficacy and safety of the CRTh2 antagonist AZD1981 as add-on therapy to inhaled corticosteroids and long-acting βDrug design, development and therapy · 2018Trial
- Increased density of intraepithelial mast cells in patients with exercise-induced bronchoconstriction regulated through epithelially derived thymic stromal lymphopoietin and IL-33.The Journal of allergy and clinical immunology · 2014Trial
- Nasal Epithelial Immune Signatures Are Associated With Age-Dependent Asthma Trajectories in Early Life.Allergy · 2026Observational
- Beyond type 2 inflammation: An innate-myeloid axis is linked to recurrence of chronic rhinosinusitis with nasal polyps.The Journal of allergy and clinical immunology · 2026Article
- Mast cells shape early pulmonary inflammation and regulate dendritic cell abundance and localization after chemical induced lung injury.Frontiers in immunology · 2026Article
- Mast cells are key mediators in the pulmonary inflammatory response to formaldehyde exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- Transcriptional Regulation of Mouse Mast Cell Differentiation and the Role of Human Lung Mast Cells in Airway Inflammation.Immunological reviews · 2025Review
- Thymic stromal lymphopoietin as a therapeutic target in patients with chronic rhinosinusitis and nasal polyps.Clinical and experimental immunology · 2025Review
- Human intraepithelial mast cell differentiation and effector function are directed by TGF-β signaling.The Journal of clinical investigation · 2025Article
- Advances in PGD2/PTGDR2 signaling pathway in tumors: A review.Biomolecules & biomedicine · 2024Review
- Article
- Mast Cells in Aspirin-Exacerbated Respiratory Disease.Current allergy and asthma reports · 2024Review
- Eosinophilic esophagitis in the "atopic march": dupilumab as an "umbrella" strategy for multiple coexisting atopic diseases.Frontiers in medicine · 2024Review
- Immunologic aspects of asthma: from molecular mechanisms to disease pathophysiology and clinical translation.Frontiers in immunology · 2024Review
- Histamine-releasing factor in severe asthma and rhinovirus-associated asthma exacerbation.The Journal of allergy and clinical immunology · 2023Article
- Aspirin-exacerbated respiratory disease: Updates in the era of biologics.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2023Review
- Mast Cells as a Potential Target of Molecular Hydrogen in Regulating the Local Tissue Microenvironment.Pharmaceuticals (Basel, Switzerland) · 2023Review
79 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 9 institutions in 1 country.
Funding
Abstract
rationaleSevere asthma (SA) remains poorly understood. Mast cells (MC) are implicated in asthma pathogenesis, but it remains unknown how their phenotype, location, and activation relate to asthma severity.
objectivesTo compare MC-related markers measured in bronchoscopically obtained samples with clinically relevant parameters between normal subjects and subjects with asthma to clarify their pathobiologic importance.
methodsEndobronchial biopsies, epithelial brushings, and bronchoalveolar lavage were obtained from subjects with asthma and normal subjects from the Severe Asthma Research Program (N = 199). Tryptase, chymase, and carboxypeptidase A (CPA)3 were used to identify total MC (MC(Tot)) and the MC(TC) subset (MCs positive for both tryptase and chymase) using immunostaining and quantitative real-time polymerase chain reaction. Lavage was analyzed for tryptase and prostaglandin D2 (PGD2) by ELISA. MEASUREMENTS AND MAIN
resultsSubmucosal MC(Tot) (tryptase-positive by immunostaining) numbers were highest in "mild asthma/no inhaled corticosteroid (ICS) therapy" subjects and decreased with greater asthma severity (P = 0.002). In contrast, MC(TC) (chymase-positive by immunostaining) were the predominant (MC(TC)/MC(Tot) > 50%) MC phenotype in SA (overall P = 0.005). Epithelial MC(Tot) were also highest in mild asthma/no ICS, but were not lower in SA. Instead, they persisted and were predominantly MC(TC). Epithelial CPA3 and tryptase mRNA supported the immunostaining data (overall P = 0.008 and P = 0.02, respectively). Lavage PGD2 was higher in SA than in other steroid-treated groups (overall P = 0.02), whereas tryptase did not differentiate the groups. In statistical models, PGD2 and MC(TC)/MC(Tot) predicted SA.
conclusionsSevere asthma is associated with a predominance of MC(TC) in the airway submucosa and epithelium. Activation of those MC(TC) may contribute to the increases in PGD2 levels. The data suggest an altered and active MC population contributes to SA pathology.
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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.