2f:I[703058,["/_next/static/immutable/chunks/3bhq_5eh1d760.js","/_next/static/immutable/chunks/1855-ogyi8eh4.js","/_next/static/immutable/chunks/2pfsjpn6k6zlg.js","/_next/static/immutable/chunks/26c7v3_3uwnwu.js","/_next/static/immutable/chunks/25a3ozcrvi1ff.js","/_next/static/immutable/chunks/2r4wx50nvjh_4.js","/_next/static/immutable/chunks/23fsw06hsi5b1.js","/_next/static/immutable/chunks/06_yt270h41rg.js","/_next/static/immutable/chunks/3ezsiz-7shkna.js","/_next/static/immutable/chunks/20x2y96ldu5wx.js","/_next/static/immutable/chunks/2lxntcm3pd1_h.js","/_next/static/immutable/chunks/00dgco8irq3jw.js","/_next/static/immutable/chunks/00nwe-kq0rboc.js","/_next/static/immutable/chunks/2051ffx3xzio9.js"],"PaperListPageClient"] 30:T71c,Non-steroidal anti-inflammatory drug-exacerbated respiratory disease (N-ERD) is characterised by the clinical triad of hypersensitivity to NSAIDs, nasal polyposis, and asthma. The cells and mediators causing acute symptoms when driving the hypersensitivity reaction to acetylsalicylic acid (ASA) ingestion, remain poorly defined. To investigate the dynamics of nasal mediators during ASA provocation in N-ERD patients before and 24 weeks after therapy with the IL-4 receptor alpha-blocking antibody dupilumab (EudraCT (2019-004889-18) and ClinicalTrials.gov (NCT04442256)). Nasal mucosal lining fluids of patients with N-ERD, chronic rhinosinusitis patients with nasal polyp (CRSwNP) and healthy disease controls were collected at selected time points up to 2 h after ASA provocation. Analysis of thirty-three different inflammatory mediators as well as transcriptomic profiling was performed. In N-ERD patients, provocation was repeated after 24 weeks of dupilumab therapy. Sixty minutes after provocation with ASA, N-ERD patients showed a significant increase in type 2 associated cytokines (i.e., TSLP, IL-5 and eotaxin-3) as compared to the other patient groups. This effect was diminished after 24 weeks of dupilumab therapy and was independent of the development of ASA tolerance. Transcriptomics revealed dampened upregulation of type 2 associated pathway genes (i.e., AREG) as well as enhanced downregulation of lipid (i.e., ALOX15) and peroxisome metabolisms (i.e., NOS2) at ASA provocation after dupilumab therapy. Treatment with dupilumab leads to reduced nasal type 2 cytokine secretion and distinct changes in transcriptomic profile during ASA provocation, but changes in type 2 mediators show no association with tolerance development. EudraCT (2019-004889-18) and ClinicalTrials.gov (NCT04442256).31:Td9d,ABSTRACT Background Non‐steroidal anti‐inflammatory drug‐exacerbated respiratory disease (N‐ERD) is characterised by the clinical triad of hypersensitivity to NSAIDs, nasal polyposis, and asthma. The cells and mediators causing acute symptoms when driving the hypersensitivity reaction to acetylsalicylic acid (ASA) ingestion, remain poorly defined. Objective To investigate the dynamics of nasal mediators during ASA provocation in N‐ERD patients before and 24 weeks after therapy with the IL‐4 receptor alpha‐blocking antibody dupilumab (EudraCT (2019‐004889‐18) and ClinicalTrials.gov (NCT04442256)). Methods Nasal mucosal lining fluids of patients with N‐ERD, chronic rhinosinusitis patients with nasal polyp (CRSwNP) and healthy disease controls were collected at selected time points up to 2 h after ASA provocation. Analysis of thirty‐three different inflammatory mediators as well as transcriptomic profiling was performed. In N‐ERD patients, provocation was repeated after 24 weeks of dupilumab therapy. Results Sixty minutes after provocation with ASA, N‐ERD patients showed a significant increase in type 2 associated cytokines (i.e., TSLP, IL‐5 and eotaxin‐3) as compared to the other patient groups. This effect was diminished after 24 weeks of dupilumab therapy and was independent of the development of ASA tolerance. Transcriptomics revealed dampened upregulation of type 2 associated pathway genes (i.e., AREG ) as well as enhanced downregulation of lipid (i.e., ALOX15 ) and peroxisome metabolisms (i.e., NOS2 ) at ASA provocation after dupilumab therapy. Conclusion and Clinical Relevance Treatment with dupilumab leads to reduced nasal type 2 cytokine secretion and distinct changes in transcriptomic profile during ASA provocation, but changes in type 2 mediators show no association with tolerance development. Trial Registration EudraCT (2019‐004889‐18) and ClinicalTrials.gov (NCT04442256) 25:[[["$","script","0",{"type":"application/ld+json","dangerouslySetInnerHTML":{"__html":"{\"@context\":\"https://schema.org\",\"@type\":\"CollectionPage\",\"name\":\"NSAID-Exacerbated Respiratory Disease: condition Research & Clinical Takeaways\",\"description\":\"Explore peer-reviewed papers on NSAID-Exacerbated Respiratory Disease (condition). Clinician-written summaries and actionable practice insights. 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Denominators differ across outcomes (e.g., n=519 for disease control vs. n=621 enrolled), suggesting some missing follow-up data.","value_numeric":null}],"summaries":{"what_studied":"This real-life, multicentre, ambispective phase 4 study evaluated the effectiveness and safety of mepolizumab 100 mg every 4 weeks in 621 adults with severe, uncontrolled chronic rhinosinusitis with nasal polyps (CRSwNP) across 25 Italian tertiary rhinology centres over 12 months.","key_result":"At 12 months, both nasal polyp score and SNOT-22 dropped significantly from baseline (p<0.0001); disease control was achieved in 42% (206/519) of patients, and 20% (104/519) were on the way to remission. However, 38% (186/495) of patients remained anosmic. Adverse events occurred in only 5% (29/621) of patients, mostly grade 1.","limitations":"- Ambispective design (partly retrospective) with no control arm limits causal inference.\n- Study limited to Italian tertiary centres, which may reduce generalisability to other settings or less-severe populations.\n- Only 12-month data are presented; remission requires a full 12-month sustained period, so true remission rates cannot yet be determined.","practice_takeaway":"Mepolizumab produces meaningful, progressive improvements in polyp burden and quality of life over 12 months in severe CRSwNP, with a good safety profile, but nearly 4 in 10 patients remain anosmic at one year. Patients with lower baseline nasal polyp scores are most likely to progress toward remission, which may help guide expectations when counselling patients."}},{"doi":"10.1016/j.jaci.2026.07.018","pmid":"42567484","title":"Beyond Type 2 Inflammation: An Innate-Myeloid Axis is Linked to CRSwNP Recurrence","journal_title":"Journal of Allergy and Clinical Immunology","journal_issn":"0091-6749","published_at":"2026-08-07T00:00:00.000Z","url":"https://doi.org/10.1016/j.jaci.2026.07.018","source_score":1,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-08-13T13:22:51.473Z","updated_at":"2026-08-13T13:22:51.473Z","tags":[{"paper_doi":"10.1016/j.jaci.2026.07.018","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.07.018","tag_type":"brand","value":"Dupixent","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.07.018","tag_type":"category","value":"Allergy","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.07.018","tag_type":"condition","value":"Chronic Rhinosinusitis With Nasal Polyps","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.07.018","tag_type":"condition","value":"NSAID-Exacerbated Respiratory Disease","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.07.018","tag_type":"generic","value":"dupilumab","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.07.018","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.07.018","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.07.018","tag_type":"modality","value":"IL-4/IL-13 Receptor Blocker","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.07.018","tag_type":"sample_size","value":"n=108","value_numeric":108},{"paper_doi":"10.1016/j.jaci.2026.07.018","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.07.018","tag_type":"study_design","value":"Retrospective Cohort Study with Prospective Validation Cohort","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.07.018","tag_type":"warning","value":"Sex distribution is not explicitly reported in the abstract; 'mixed' sex tag is inferred from general CRSwNP population norms.","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.07.018","tag_type":"warning","value":"The 'practice_changing' impact flag is applied cautiously — findings are hypothesis-generating and not yet validated in a prospective interventional trial.","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.07.018","tag_type":"warning","value":"The retrospective cohort (n=91) and the dupilumab cohort (n=17) are separate populations; direct comparisons between them should be interpreted cautiously.","value_numeric":null},{"paper_doi":"10.1016/j.jaci.2026.07.018","tag_type":"warning","value":"The study used nasal fluid (not tissue) to track dupilumab effects, which may not fully reflect tissue-level changes seen in the recurrence cohort.","value_numeric":null}],"summaries":{"what_studied":"This study examined tissue-based biomarkers predicting post-FESS CRSwNP recurrence in 91 patients (dichotomized as rapid recurrence <1 year vs. slow/no recurrence >2 years), and assessed whether dupilumab modifies these mediators in a separate prospective cohort of 17 CRSwNP patients over 2 months.","key_result":"23 tissue mediators predicted rapid recurrence (AUC >0.70), spanning T2 markers (IL-4, IL-13, IgE) and innate/myeloid markers (CCL3/4/7/8/13, CSF2, IL-1β, MMP12, HIF-1α, TNF-α); dupilumab reduced T2-linked mediators (IL-5Rα, CCL3, CCL4, CCL13) but left key myeloid mediators unchanged (CCL8, CSF2, IL-1β, MMP12, HIF-1α).","limitations":"Retrospective design for the recurrence cohort introduces selection bias; the dupilumab cohort was small (n=17) and only followed for 2 months; nasal fluid rather than tissue was used to assess dupilumab effects, limiting direct comparability.","practice_takeaway":"Clinicians should recognize that dupilumab does not suppress a parallel innate/myeloid inflammatory axis in CRSwNP, which may drive recurrence after T2 blockade is stopped or insufficient. Myeloid mediators like CSF2, IL-1β, and MMP12 are candidate targets worth monitoring in patients with rapid post-FESS recurrence."}},{"doi":"10.1111/cea.70184","pmid":"41309110","title":"Dupilumab Dampens Mucosal Type 2 Response During Acetylsalicylic Acid Challenge in N‐ERD Patients","journal_title":"Clinical & Experimental Allergy","journal_issn":"0954-7894","published_at":"2025-11-28T00:00:00.000Z","url":"https://doi.org/10.1111/cea.70184","source_score":1,"is_retracted":false,"is_open_access":true,"raw_metadata":{"ooir":{"day":"2025-11-30","doi":"10.1111/cea.70184","days":"7","issn":"0954-7894","rank":"9","field":"Clinical Medicine","score":"1","category":"Allergy","categories":["Allergy"],"_categories":["Allergy"]},"pubmed":{"doi":"10.1111/cea.70184","title":"Dupilumab Dampens Mucosal Type 2 Response During Acetylsalicylic Acid Challenge in N-ERD Patients.","journal":"Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology","methods":"","results":"Sixty minutes after provocation with ASA, N-ERD patients showed a significant increase in type 2 associated cytokines (i.e., TSLP, IL-5 and eotaxin-3) as compared to the other patient groups. This effect was diminished after 24 weeks of dupilumab therapy and was independent of the development of ASA tolerance. Transcriptomics revealed dampened upregulation of type 2 associated pathway genes (i.e., AREG) as well as enhanced downregulation of lipid (i.e., ALOX15) and peroxisome metabolisms (i.e., NOS2) at ASA provocation after dupilumab therapy.","abstract":"$30","keywords":["aspirin‐induced asthma","chronic rhinosinusitis","nasal polyposis","type 2 inflammation"],"pubmed_id":"41309110","conclusions":"","publication_date":"2025-11-28T00:00:00"},"crossref":{"DOI":"10.1111/cea.70184","URL":"https://doi.org/10.1111/cea.70184","ISSN":["0954-7894","1365-2222"],"link":[{"URL":"https://onlinelibrary.wiley.com/doi/pdf/10.1111/cea.70184","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"page":null,"type":"journal-article","issue":null,"score":1,"title":["Dupilumab Dampens Mucosal Type 2 Response During Acetylsalicylic Acid Challenge in N‐ERD Patients"],"author":[{"given":"Julia","family":"Eckl‐Dorna","sequence":"first","affiliation":[{"name":"Department of Otorhinolaryngology General Hospital and Medical University of Vienna Vienna Austria"}]},{"given":"Christina","family":"Morgenstern","sequence":"additional","affiliation":[{"name":"Department of Otorhinolaryngology General Hospital and Medical University of Vienna Vienna Austria"}]},{"given":"Katharina","family":"Poglitsch","sequence":"additional","affiliation":[{"name":"Department of Dermatology General Hospital and Medical University of Vienna Vienna Austria"}]},{"given":"Tamara","family":"Arnoldner","sequence":"additional","affiliation":[{"name":"Department of Dermatology General Hospital and Medical University of Vienna Vienna Austria"}]},{"given":"Katharina","family":"Gangl","sequence":"additional","affiliation":[{"name":"Department of Otorhinolaryngology General Hospital and Medical University of Vienna Vienna Austria"}]},{"given":"Tina J.","family":"Bartosik","sequence":"additional","affiliation":[{"name":"Department of Otorhinolaryngology General Hospital and Medical University of Vienna Vienna Austria"}]},{"given":"Nicholas J.","family":"Campion","sequence":"additional","affiliation":[{"name":"Department of Otorhinolaryngology General Hospital and Medical University of Vienna Vienna Austria"}]},{"given":"Aldine","family":"Tu","sequence":"additional","affiliation":[{"name":"Department of Otorhinolaryngology General Hospital and Medical University of Vienna Vienna Austria"}]},{"given":"Victoria","family":"Stanek","sequence":"additional","affiliation":[{"name":"Department of Otorhinolaryngology General Hospital and Medical University of Vienna Vienna Austria"}]},{"given":"Sven","family":"Schneider","sequence":"additional","affiliation":[{"name":"Department of Otorhinolaryngology General Hospital and Medical University of Vienna Vienna Austria"}]},{"given":"Christine","family":"Bangert","sequence":"additional","affiliation":[{"name":"Department of Dermatology General Hospital and Medical University of Vienna Vienna Austria"}]}],"issued":{"date-parts":[[2025,11,27]]},"member":"311","prefix":"10.1111","source":"Crossref","volume":null,"archive":["Portico"],"created":{"date-time":"2025-11-28T00:44:38Z","timestamp":1764290678000,"date-parts":[[2025,11,28]]},"indexed":{"date-time":"2025-11-28T00:47:34Z","timestamp":1764290854015,"date-parts":[[2025,11,28]]},"license":[{"URL":"http://creativecommons.org/licenses/by-nc-nd/4.0/","start":{"date-time":"2025-11-27T00:00:00Z","timestamp":1764201600000,"date-parts":[[2025,11,27]]},"delay-in-days":0,"content-version":"vor"}],"subject":[],"abstract":"$31","language":"en","relation":{},"resource":{"primary":{"URL":"https://onlinelibrary.wiley.com/doi/10.1111/cea.70184"}},"subtitle":[],"assertion":[{"name":"received","group":{"name":"publication_history","label":"Publication History"},"label":"Received","order":0,"value":"2025-04-07"},{"name":"accepted","group":{"name":"publication_history","label":"Publication History"},"label":"Accepted","order":2,"value":"2025-11-12"},{"name":"published","group":{"name":"publication_history","label":"Publication History"},"label":"Published","order":3,"value":"2025-11-27"}],"deposited":{"date-time":"2025-11-28T00:44:44Z","timestamp":1764290684000,"date-parts":[[2025,11,28]]},"issn-type":[{"type":"print","value":"0954-7894"},{"type":"electronic","value":"1365-2222"}],"published":{"date-parts":[[2025,11,27]]},"publisher":"Wiley","reference":[{"DOI":"10.1111/all.13599","key":"e_1_2_11_2_1","year":"2019","issue":"1","author":"Kowalski M. 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