ArticleScientific reports2021
Interleukin-33 and thymic stromal lymphopoietin, but not interleukin-25, are crucial for development of airway eosinophilia induced by chitin.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Chitin Is a Potent Inducer of Type 2 Airway Inflammation Independent of Endogenous Chitinolytic Activity.Allergy · 2026Article
- Quercetin modulates mast cell activation and the IL-33/ST2/NF-κB axis in allergic rhinitis.Scientific reports · 2026Article
- The rhinovirus puzzle: Linking virus and host factors to childhood asthma.The Journal of allergy and clinical immunology · 2026Review
- Integrated airway epithelial signaling networks linking allergen-driven inflammation to airway remodeling in asthma.Frontiers in immunology · 2026Review
- ILC2 Diversity, Location, and Function in Pulmonary Disease.Immunological reviews · 2025Review
- Fungal chitin is not an independent mediator of allergic fungal asthma severity.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- From the bench to the clinic: basophils and type 2 epithelial cytokines of thymic stromal lymphopoietin and IL-33.Clinical & translational immunology · 2024Review
- Interleukin-33 increases type 2 innate lymphoid cell count and their activation in eosinophilic asthma.Clinical and translational allergy · 2023Article
- Immunologic, genetic, and ecological interplay of factors involved in allergic diseases.Frontiers in allergy · 2023Review
- IL-24 Contributes to Neutrophilic Asthma in an IL-17A-Dependent Manner and Is Suppressed by IL-37.Allergy, asthma & immunology research · 2022Article
- ILCs and Allergy.Advances in experimental medicine and biology · 2022Article
- Functional Contribution and Targeted Migration of Group-2 Innate Lymphoid Cells in Inflammatory Lung Diseases: Being at the Right Place at the Right Time.Frontiers in immunology · 2021Review
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Authors and funding
15 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Exposure to various antigens derived from house dust mites (HDM) is considered to be a risk factor for development of certain allergic diseases such as atopic asthma, atopic dermatitis, rhinitis and conjunctivitis. Chitin is an insoluble polysaccharide (β-(1-4)-poly-N-acetyl-D-glucosamine) and a major component in the outer shell of HDMs. Mice exposed to chitin develop asthma-like airway eosinophilia. On the other hand, several lines of evidence show that the effects of chitin on immune responses are highly dependent on the size of chitin particles. In the present study, we show that chitin induced production of IL-33 and TSLP by alveolar and bronchial epithelial cells, respectively, in mice. IL-25, IL-33 and TSLP were reported to be important for group 2 innate lymphoid cell (ILC2)-, but not Th2 cell-, dependent airway eosinophilia in a certain model using chitin beads. Here, we show that-in our murine models-epithelial cell-derived IL-33 and TSLP, but not IL-25, were crucial for activation of resident lung Th2 cells as well as group 2 innate lymphoid cells (ILC2s) to produce IL-5, resulting in development of chitin-induced airway eosinophilia. Our findings provide further insight into the underlying mechanisms of development of HDM-mediated allergic disorders.
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