Trial reportThe Journal of allergy and clinical immunology2015
Pediatric severe asthma with fungal sensitization is mediated by steroid-resistant IL-33.
Trial report in The Journal of allergy and clinical immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis 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.
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
88 citing papers in PubMed, 1 synthesis or guideline pooled it, 196 citations in OpenAlex.
- Pooled it
- From Susceptibility to Severity: The Impact of Interleukin-33 rs1929992 Polymorphism on Asthma in a Taiwanese Population.Life (Basel, Switzerland) · 2026Article
- Evidence-Based Clinical Recommendations for the Appropriate Use of Diagnostic Tests in Pediatric Allergology: Focus on Asthma, Rhinoconjunctivitis, and Keratoconjunctivitis Vernal.Journal of clinical medicine · 2026Review
- The Airway Epithelial Barrier in Childhood Asthma: A Central Player in Glucocorticoid Therapy, Resistance, and Severe Asthma.Pediatric discovery · 2026Review
- Fine-Tuning Group 2 Innate Lymphoid Cells: CD48 Pumps Up the Volume.American journal of respiratory cell and molecular biology · 2026Article
- Animal models of fungus-related allergic airway disease: exposures, readouts, mechanisms, and translational gaps.Frontiers in cellular and infection microbiology · 2026Review
- Mechanistic modelling of allergen-induced airways disease in early life.Scientific reports · 2025Article
- Mast cell activation disrupts interactions between endothelial cells and pericytes during early life allergic asthma.The Journal of clinical investigation · 2024Article
- Investigations of a combination of atopic status and age of asthma onset identify asthma subphenotypes.The Journal of asthma : official journal of the Association for the Care of Asthma · 2023Article
- Effects of Allergen Exposure and Environmental Risk Factors in Schools on Childhood Asthma.Current allergy and asthma reports · 2023Review
- The modulation of pulmonary group 2 innate lymphoid cell function in asthma: from inflammatory mediators to environmental and metabolic factors.Experimental & molecular medicine · 2023Review
- Novel mechanistic insights underlying fungal allergic inflammation.PLoS pathogens · 2023Review
- Diet-induced obesity worsens allergen-induced type 2/type 17 inflammation in airways by enhancing DUOX1 activation.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Severe Fungal Asthma: A Role for Biologics and Inhaled Antifungals.Journal of fungi (Basel, Switzerland) · 2023Article
- Differential protease content of mast cells and the processing of IL-33 inFrontiers in immunology · 2023Article
- Sterols in asthma.Trends in immunology · 2022Review
- Review
- Endothelin-A Receptor Antagonist Alleviates Allergic Airway InflammationFrontiers in immunology · 2022Article
- Modulating ILC2 function for treatment of type 2 airway diseases.Current trends in immunology · 2022Article
- Crosstalk between ILC2s and Th2 CD4Journal of immunology research · 2022Review
28 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
17 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundThe mechanism underlying severe asthma with fungal sensitization (SAFS) is unknown. IL-33 is important in fungus-induced asthma exacerbations, but its role in fungal sensitization is unexplored.
objectiveWe sought to determine whether fungal sensitization in children with severe therapy-resistant asthma is mediated by IL-33.
methodsEighty-two children (median age, 11.7 years; 63% male) with severe therapy-resistant asthma were included. SAFS (n = 38) was defined as specific IgE or skin prick test response positivity to Aspergillus fumigatus, Alternaria alternata, or Cladosporium herbarum. Clinical features and airway immunopathology were assessed. Chronic exposure to house dust mite and A alternata were compared in a neonatal mouse model.
resultsChildren with SAFS had earlier symptom onset (0.5 vs 1.5 years, P = .006), higher total IgE levels (637 vs 177 IU/mL, P = .002), and nonfungal inhalant allergen-specific IgE. Significantly more children with SAFS were prescribed maintenance oral steroids (42% vs 14%, P = .02). SAFS was associated with higher airway IL-33 levels. In neonatal mice A alternata exposure induced higher serum IgE levels, pulmonary IL-33 levels, and IL-13(+) innate lymphoid cell (ILC) and TH2 cell numbers but similar airway hyperresponsiveness (AHR) compared with those after house dust mite exposure. Lung IL-33 levels, IL-13(+) ILC numbers, TH2 cell numbers, IL-13 levels, and AHR remained increased with inhaled budesonide during A alternata exposure, but all features were significantly reduced in ST2(-/-) mice lacking a functional receptor for IL-33.
conclusionPediatric SAFS was associated with more oral steroid therapy and higher IL-33 levels. A alternata exposure resulted in increased IL-33-mediated ILC2 numbers, TH2 cell numbers, and steroid-resistant AHR. IL-33 might be a novel therapeutic target for SAFS.
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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.