ArticleThe Journal of allergy and clinical immunology2013
Prominent role of IFN-γ in patients with aspirin-exacerbated respiratory disease.
Article in The Journal of allergy and clinical immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
51 citing papers in PubMed, 96 citations in OpenAlex.
- Decreased expression of type I (IFN-β) and type III (IFN-λ) interferons and interferon-stimulated genes in patients with chronic rhinosinusitis with and without nasal polyps.The Journal of allergy and clinical immunology · 2019Trial
- Aspirin activation of eosinophils and mast cells: implications in the pathogenesis of aspirin-exacerbated respiratory disease.Journal of immunology (Baltimore, Md. : 1950) · 2014Trial
- Differential regulation of 5-lipoxygenase and leukotriene-C4-synthase expression by IFNγ, IL-4 and IL-13 in human monocytes and macrophages from patients with atopic dermatitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Sputum Eosinophil and Macrophage Changes After Aspirin Challenge in Patients With Nonsteroidal Anti-Inflammatory Drug-Exacerbated Respiratory Disease.Clinical and translational allergy · 2025Article
- Sleep dysfunction in aspirin exacerbated respiratory disease: A prospective cohort study.World journal of otorhinolaryngology - head and neck surgery · 2025Article
- Review
- Common Cold Coronavirus 229E Induces Higher Interferon Stimulating Gene Responses in Human Nasal Epithelial Cells from Patients with Chronic Rhinosinusitis with Polyposis.American journal of rhinology & allergy · 2025Article
- Inflammatory profile of eosinophils in asthma-COPD overlap and eosinophilic COPD: a multi-omics study.Frontiers in immunology · 2024Article
- Nonsteroidal antiinflammatory drug-exacerbated respiratory disease: molecular mechanism, management and treatment.Frontiers in allergy · 2024Review
- Increased epithelial mTORC1 activity in chronic rhinosinusitis with nasal polyps.bioRxiv : the preprint server for biology · 2023Article
- Non-eosinophilic asthma in nonsteroidal anti-inflammatory drug exacerbated respiratory disease.Clinical and translational allergy · 2023Article
- Local and Systemic Production of Pro-Inflammatory Eicosanoids Is Inversely Related to Sensitization to Aeroallergens in Patients with Aspirin-Exacerbated Respiratory Disease.Journal of personalized medicine · 2022Article
- Emerging Biomarkers Beyond Leukotrienes for the Management of Nonsteroidal Anti-inflammatory Drug (NSAID)-Exacerbated Respiratory Disease.Allergy, asthma & immunology research · 2022Review
- The Role of Defective Epithelial Barriers in Allergic Lung Disease and Asthma Development.Journal of asthma and allergy · 2022Review
- Carbon dioxide inhibits COVID-19-type proinflammatory responses through extracellular signal-regulated kinases 1 and 2, novel carbon dioxide sensors.Cellular and molecular life sciences : CMLS · 2021Article
- Epithelial dysregulation in chronic rhinosinusitis with nasal polyposis (CRSwNP) and aspirin-exacerbated respiratory disease (AERD).The Journal of allergy and clinical immunology · 2021Article
- Innate immune cell dysregulation drives inflammation and disease in aspirin-exacerbated respiratory disease.The Journal of allergy and clinical immunology · 2021Review
- Inflammatory heterogeneity in aspirin-exacerbated respiratory disease.The Journal of allergy and clinical immunology · 2021Article
- Lipid-mediated innate lymphoid cell recruitment and activation in aspirin-exacerbated respiratory disease.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2021Review
- Phosphoproteomics identifies microglial Siglec-F inflammatory response during neurodegeneration.Molecular systems biology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAspirin-exacerbated respiratory disease (AERD) is distinguished from aspirin-tolerant asthma/chronic sinusitis in large part by an exuberant infiltration of eosinophils that are characterized by their overexpression of metabolic pathways that drive the constitutive and aspirin-induced secretion of cysteinyl leukotrienes (CysLTs).
objectiveWe defined the inflammatory milieu that in part drives CysLT overproduction and, in particular, the role of IFN-γ in the differentiation of eosinophils.
methodsQuantitative real-time PCR was performed for TH1 and TH2 signature cytokines on tissue from control subjects, patients with chronic hyperplastic eosinophilic sinusitis, and patients with AERD, and their cellular source was determined. The influence of IFN-γ on maturation, differentiation, and functionality of eosinophils derived from hematopoietic stem cells was determined.
resultsGene expression analysis revealed that tissue from both aspirin-tolerant subjects and patients with AERD display a TH2 cytokine signature; however, AERD was distinguished from chronic hyperplastic eosinophilic sinusitis by the prominent expression of IFN-γ. Intracellular and immunohistochemical cytokine staining revealed that the major sources of these cytokines were the eosinophils themselves. IFN-γ promoted the maturation of eosinophil progenitors, as measured by increased mRNA and surface expression of CCR3 and sialic acid-binding immunoglobulin-like lectin 8 (Siglec-8). Additionally, IFN-γ increased the expression of genes involved in leukotriene synthesis that led to increased secretion of CysLTs. IFN-γ-matured eosinophil progenitors were also primed, as demonstrated by their enhanced degranulation.
conclusionsHigh IFN-γ levels distinguish AERD from aspirin-tolerant asthma and underlie the robust constitutive and aspirin-induced secretion of CysLTs that characterize this disorder.
Indexed as
Identifiers
What OpenQuestion holds
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.