ArticleAllergy2026
Club Cells in Nasal Epithelial Repair: Insights From an IL-13-Induced Inflammatory Model.
Article in Allergy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The trial behind it
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Who cites it
5 citing papers in PubMed.
- Restoring the Airway Barrier: How Targeting Eosinophilic Inflammation Shapes Epithelial Health and Clinical Remission in Asthma.Diagnostics (Basel, Switzerland) · 2026Review
- Understanding Nasal Polyposis: The Roles of Ion Channels, Inflammation, Ionocytes, and Prostaglandin E2-The IJournal of clinical medicine · 2026Article
- Club Cells in Nasal Epithelial Repair: Insights From an IL-13-Induced Inflammatory Model.Allergy · 2026Article
- Oxidative Stress and PRKN-Mediated Senescence Link RhoA/ROCK Signaling to Epithelial Remodeling in Allergic Rhinitis.Antioxidants (Basel, Switzerland) · 2026Article
- Nasopharyngeal swab transcriptomics identifies divergent molecular signatures in adenoid hypertrophy and allergic rhinitis comorbidity.Frontiers in immunology · 2026Article
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
backgroundClub cells, originating from basal cells, can differentiate into ciliated or goblet cells in the lower respiratory tract, but their role in nasal epithelium during chronic rhinosinusitis with nasal polyps (CRSwNP) is not well understood. We aim to investigate the role of club cells in CRSwNP and their biological mechanism in an IL-13-induced inflammation model of human nasal epithelial cells (HNECs).
methodsCRSwNP was classified into four endotypes (N
resultsClub and ciliated cells significantly decreased in four endotypes of CRSwNP (all p < 0.001), while basal and goblet cells increased in neutrophilic and eosinophilic CRSwNP, respectively (all p < 0.05). In vitro, IL-13-induced significant cilia loss and MUC5AC secretion compared to IFN-γ and IL-17A (all p < 0.05), and FCM revealed a shift from SCGB1A1
conclusionsClub cells are crucial in nasal epithelial repair, which is notably compromised in CRSwNP. This impairment is highlighted in an IL-13-induced inflammation model of nasal epithelium and further underscored by the therapeutic effect of Dupilumab in restoring epithelial repair mechanisms.
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