ArticleThe Journal of clinical investigation1998
Overexpression of leukotriene C4 synthase in bronchial biopsies from patients with aspirin-intolerant asthma.
Article in The Journal of clinical investigation, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 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
106 citing papers in PubMed, 2 syntheses or guidelines pooled it, 552 citations in OpenAlex.
- Contemporary management of chronic rhinosinusitis with nasal polyposis in aspirin-exacerbated respiratory disease: an evidence-based review with recommendations.International forum of allergy & rhinology · 2016Pooled it
- The use of analgesics in patients with asthma.Drug safety · 2001Pooled it
- A trial of type 12 purinergic (P2YThe Journal of allergy and clinical immunology · 2019Trial
- Aspirin-Exacerbated Respiratory Disease Involves a Cysteinyl Leukotriene-Driven IL-33-Mediated Mast Cell Activation Pathway.Journal of immunology (Baltimore, Md. : 1950) · 2015Trial
- Biological effects of leukotriene E4 on eosinophils.Prostaglandins, leukotrienes, and essential fatty acids · 2014Trial
- Aspirin activation of eosinophils and mast cells: implications in the pathogenesis of aspirin-exacerbated respiratory disease.Journal of immunology (Baltimore, Md. : 1950) · 2014Trial
- Trial
- Trial
- Toward precision medicine in nonsteroidal anti-inflammatory drug-exacerbated respiratory disease.ERJ open research · 2026Article
- Updating the classification and routine diagnosis of NSAID hypersensitivity reactions: A WAO Statement.The World Allergy Organization journal · 2025Review
- Differential Analysis of Hemogram Parameters and Cellular Ratios in Severe Asthma Exacerbations: A Comparative Study of Eosinophilic and Non-Eosinophilic Phenotypes.Life (Basel, Switzerland) · 2025Article
- Clinical and mechanistic advancements in aspirin exacerbated respiratory disease.The Journal of allergy and clinical immunology · 2025Review
- New insights into the mechanisms of aspirin-exacerbated respiratory disease.Current opinion in allergy and clinical immunology · 2025Review
- Cysteinyl Leukotrienes in Allergic Inflammation.Annual review of pathology · 2025Review
- Low Prostaglandin EJournal of clinical medicine · 2024Review
- Mast Cells in Aspirin-Exacerbated Respiratory Disease.Current allergy and asthma reports · 2024Review
- Updates on immune mechanisms in aspirin-exacerbated respiratory disease.The Journal of allergy and clinical immunology · 2023Review
- Article
- Emerging Biomarkers Beyond Leukotrienes for the Management of Nonsteroidal Anti-inflammatory Drug (NSAID)-Exacerbated Respiratory Disease.Allergy, asthma & immunology research · 2022Review
- Innate immune cell dysregulation drives inflammation and disease in aspirin-exacerbated respiratory disease.The Journal of allergy and clinical immunology · 2021Review
46 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
11 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aspirin causes bronchoconstriction in aspirin-intolerant asthma (AIA) patients by triggering cysteinyl-leukotriene (cys-LT) production, probably by removing PGE2-dependent inhibition. To investigate why aspirin does not cause bronchoconstriction in all individuals, we immunostained enzymes of the leukotriene and prostanoid pathways in bronchial biopsies from AIA patients, aspirin-tolerant asthma (ATA) patients, and normal (N) subjects. Counts of cells expressing the terminal enzyme for cys-LT synthesis, LTC4 synthase, were fivefold higher in AIA biopsies (11.5+/-2.2 cells/mm2, n = 10) than in ATA biopsies (2.2+/-0.7, n = 10; P = 0. 0006) and 18-fold higher than in N biopsies (0.6+/-0.4, n = 9; P = 0. 0002). Immunostaining for 5-lipoxygenase, its activating protein (FLAP), LTA4 hydrolase, cyclooxygenase (COX)-1, and COX-2 did not differ. Enhanced baseline cys-LT levels in bronchoalveolar lavage (BAL) fluid of AIA patients correlated uniquely with bronchial counts of LTC4 synthase+ cells (rho = 0.83, P = 0.01). Lysine-aspirin challenge released additional cys-LTs into BAL fluid in AIA patients (200+/-120 pg/ml, n = 8) but not in ATA patients (0. 7+/-5.1, n = 5; P = 0.007). Bronchial responsiveness to lysine-aspirin correlated exclusively with LTC4 synthase+ cell counts (rho = -0.63, P = 0.049, n = 10). Aspirin may remove PGE2-dependent suppression in all subjects, but only in AIA patients does increased bronchial expression of LTC4 synthase allow marked overproduction of cys-LTs leading to bronchoconstriction.
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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.