ArticlePloS one2012
Primary human airway epithelial cell-dependent inhibition of human lung mast cell degranulation.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
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Who cites it
21 citing papers in PubMed, 45 citations in OpenAlex.
- The Role of Endogenous Specialized Proresolving Mediators in Mast Cells and Their Involvement in Inflammation and Resolution.International journal of molecular sciences · 2025Review
- Lipoxin AFrontiers in immunology · 2024Article
- Distinct Epithelial-Innate Immune Cell Transcriptional Circuits Underlie Airway Hyperresponsiveness in Asthma.American journal of respiratory and critical care medicine · 2023Article
- Cellular and Molecular Signatures of Oxidative Stress in Bronchial Epithelial Cell Models Injured by Cigarette Smoke Extract.International journal of molecular sciences · 2022Review
- Human airway mast cells proliferate and acquire distinct inflammation-driven phenotypes during type 2 inflammation.Science immunology · 2021Observational
- The potential of lipid mediator networks as ocular surface therapeutics and biomarkers.The ocular surface · 2021Review
- Resolution-Based Therapies: The Potential of Lipoxins to Treat Human Diseases.Frontiers in immunology · 2021Review
- Insulin-induced lipid body accumulation is accompanied by lipid remodelling in model mast cells.Adipocyte · 2019Article
- Modulation of Mast Cell Reactivity by Lipids: The Neglected Side of Allergic Diseases.Frontiers in immunology · 2019Review
- The diversity of myeloid immune cells shaping wound repair and fibrosis in the lung.Regeneration (Oxford, England) · 2018Review
- Bronchoprotective mechanisms for specialized pro-resolving mediators in the resolution of lung inflammation.Molecular aspects of medicine · 2017Review
- Are specialized pro-resolving mediators promising therapeutic agents for severe bronchial asthma?Journal of thoracic disease · 2017Article
- Phenotypic and genetic aspects of epithelial barrier function in asthmatic patients.The Journal of allergy and clinical immunology · 2017Review
- Lipoxin AScientific reports · 2016Article
- Bronchial epithelium in children: a key player in asthma.European respiratory review : an official journal of the European Respiratory Society · 2016Review
- Mast cells in airway diseases and interstitial lung disease.European journal of pharmacology · 2016Review
- Bidirectional Counterregulation of Human Lung Mast Cell and Airway Smooth Muscle β2 Adrenoceptors.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Culture conditions profoundly impact phenotype in BEAS-2B, a human pulmonary epithelial model.Journal of applied toxicology : JAT · 2015Article
- Lipoxin B₄ promotes the resolution of allergic inflammation in the upper and lower airways of mice.Mucosal immunology · 2015Article
- Article
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
introductionChronic mast cell activation is a characteristic feature of asthma. BEAS-2B human airway epithelial cells (AEC) profoundly inhibit both constitutive and IgE-dependent human lung mast cell (HLMC) histamine release. The aim of this study was to examine the regulation of HLMC degranulation by primary AEC from healthy and asthmatic subjects, and investigate further the inhibitory mechanism.
methodsHLMC were co-cultured with both BEAS-2B and primary AEC grown as monolayers or air-liquid interface (ALI) cultures.
resultsBoth constitutive and IgE-dependent HLMC histamine release were attenuated by BEAS-2B, primary AEC monolayers and ALI cultures. This occurred in the absence of HLMC-AEC contact indicating the presence of a soluble factor. Unlike healthy ALI AEC, asthmatic ALI-AEC did not significantly reduce constitutive histamine release. AEC inhibitory activity was transferable in primary AEC monolayer supernatant, but less active than with Transwell co-culture, suggesting that the inhibitory factor was labile. The AEC inhibitory effects were attenuated by both AEC wounding and pertussis toxin, indicating the involvement of a G(0)/G(i) receptor coupled mechanism. Solid phase extraction of lipids (<10 kDa) removed the AEC inhibitory activity. The lipid derivatives resolving D1 and D2 and lipoxin A(4) attenuated HLMC histamine release in a dose-dependent fashion but were not detectable in co-culture supernatants.
conclusionsPrimary AEC suppress HLMC constitutive and IgE-dependent histamine secretion through the release of a soluble, labile lipid mediator(s) that signals through the G(0)/G(i) receptor coupled mechanism. Manipulation of this interaction may have a significant therapeutic role 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.