ReviewCurrent opinion in allergy and clinical immunology2025
New insights into the mechanisms of aspirin-exacerbated respiratory disease.
Review in Current opinion in allergy and clinical immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
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Who cites it
7 citing papers in PubMed.
- Efficacy of Biologics in Aspirin 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
- Indomethacin Abolishes the Potentiation Effect of Testosterone on the Relaxation Induced by Salbutamol and Theophylline by Directly Blocking the KMolecules (Basel, Switzerland) · 2025Article
- Clinical and mechanistic advancements in aspirin exacerbated respiratory disease.The Journal of allergy and clinical immunology · 2025Review
- Article
- Oncostatin M Drives Th2 Polarized Allergic Airway Inflammation Through Fibroblast Reprogramming and Endoplasmic Reticulum Stress.International journal of nanomedicine · 2025Article
Corrections and comments
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Authors and funding
1 author.
Funding
Abstract
purpose of reviewAspirin-exacerbated respiratory disease (AERD), a syndrome characterized clinically by asthma, chronic rhinosinusitis with nasal polyposis, and respiratory reactions to aspirin and other cyclooxygenase-1 inhibitors, is an inflammatory condition of the respiratory tract that is often severe and challenging to treat. There have been several recent advances in our understanding of the underlying pathology of the disease. These have been paralleled by welcome advances in the availability of targeted treatment options for patients with AERD. RECENT
findingsSpurred in part by results from trials of targeted biologic therapies, along with single cell genomics, there is now clear evidence that the chronic respiratory inflammation in AERD is driven by combination of local tissue factors. These include abnormalities in effector cell populations, with increased accumulation and activation of mast cells and plasma cells in the nasal polyp, along with notable epithelial barrier dysregulation. The key mediators now identified include high levels of both type 2 inflammatory cytokines (IL-4, IL-5, IL-13) and cytokines involved in broader inflammatory pathways (IL-33, TSLP, IL-6, oncostatin M), as well as the overproduction of cysteinyl leukotrienes, and the underproduction of prostaglandin E 2 . SUMMARY: This review covers the latest insights into the immunopathogenesis of and targeted treatment of AERD, including the roles of lipids, effector cells, and inflammatory cytokines, and discusses unanswered questions regarding its pathogenesis and potential future therapies.
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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.