ArticleThe Journal of allergy and clinical immunology2024
IL-4Rα signaling promotes barrier-altering oncostatin M and IL-6 production in aspirin-exacerbated respiratory disease.
Article in The Journal of allergy and clinical immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- The role of IL-6 -174C/G polymorphism in hepatitis B virus infection: a genetic association study.Journal, genetic engineering & biotechnology · 2026Article
- 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
- CD25 expression marks an activated mast cell population in human nasal polyposis.The Journal of allergy and clinical immunology · 2026Article
- Integrated Immune, Epithelial and Lipid Pathways in NSAID-Exacerbated Respiratory Disease.Clinical and translational allergy · 2026Review
- Antioxidant Enzymes Genetic Variants Associated with Urticaria/Angioedema Induced by Cross-Reactive Hypersensitivity to Nonsteroidal Anti-Inflammatory Drugs.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Biologic therapies targeting type 2 inflammation in NSAID-exacerbated respiratory disease.Frontiers in immunology · 2026Review
- Analysis of Selected Serum Cytokines to Evaluate the Early Efficacy of Benralizumab, Dupilumab, and Mepolizumab in Severe Eosinophilic Asthma Treatment.International journal of molecular sciences · 2025Article
- Nasal Epithelial Extracellular Vesicles Correlate with Type 2 Inflammation during Aspirin-induced Respiratory Reactions.American journal of respiratory cell and molecular biology · 2025Article
- Clinical efficacy and mechanisms of biologics for chronic rhinosinusitis with nasal polyps.The Journal of allergy and clinical immunology · 2025Review
- Clinical and mechanistic advancements in aspirin exacerbated respiratory disease.The Journal of allergy and clinical immunology · 2025Review
- Review
- New insights into the mechanisms of aspirin-exacerbated respiratory disease.Current opinion in allergy and clinical immunology · 2025Review
- Advances in Interleukin-6 Family Cytokines and the Role in Respiratory Diseases.Journal of inflammation research · 2025Review
- Global research trends and hotspots in aspirin studies (2014-2024): a bibliometric perspective.Frontiers in pharmacology · 2025Review
- Neutrophils in nasal polyps exhibit transcriptional adaptation and proinflammatory roles that depend on local polyp milieu.JCI insight · 2024Article
- Update on the Biological and Clinical Relevance of Mast Cells in Chronic Rhinosinusitis with Nasal Polyps.Biomedicines · 2024Review
- Efficacy of Biologics in NSAID-ERD: United Airways From the Nose to the Bronchi.The journal of allergy and clinical immunology. In practice · 2024Review
- Nonsteroidal antiinflammatory drug-exacerbated respiratory disease: molecular mechanism, management and treatment.Frontiers in allergy · 2024Review
- Pan-cancer Evaluation of the Neutrophil-to-Lymphocyte Ratio as a Prognostic Marker Across Six Major Solid Tumors.In vivo (Athens, Greece)Article
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Authors and funding
13 authors.
Funding
Abstract
backgroundAspirin-exacerbated respiratory disease (AERD) is a severe disease involving dysregulated type 2 inflammation. However, the role other inflammatory pathways play in AERD is poorly understood.
objectiveWe sought to broadly define the inflammatory milieu of the upper respiratory tract in AERD and to determine the effects of IL-4Rα inhibition on mediators of nasal inflammation.
methodsTwenty-two AERD patients treated with dupilumab for 3 months were followed over 3 visits and compared to 10 healthy controls. Nasal fluid was assessed for 45 cytokines and chemokines using Olink Target 48. Blood neutrophils and cultured human mast cells, monocytes/macrophages, and nasal fibroblasts were assessed for response to IL-4/13 stimulation in vitro.
resultsOf the nasal fluid cytokines measured, nearly one third were higher in AERD patients compared to healthy controls, including IL-6 and the IL-6 family-related cytokine oncostatin M (OSM), both of which correlated with nasal albumin levels, a marker of epithelial barrier dysregulation. Dupilumab significantly decreased many nasal mediators, including OSM and IL-6. IL-4 stimulation induced OSM production from mast cells and macrophages but not from neutrophils, and OSM and IL-13 stimulation induced IL-6 production from nasal fibroblasts.
conclusionIn addition to type 2 inflammation, innate and IL-6-related cytokines are also elevated in the respiratory tract in AERD. Both OSM and IL-6 are locally produced in nasal polyps and likely promote pathology by negatively affecting epithelial barrier function. IL-4Rα blockade, although seemingly directed at type 2 inflammation, also decreases mediators of innate inflammation and epithelial dysregulation, which may contribute to dupilumab's therapeutic efficacy in AERD.
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