ArticleThe Journal of clinical investigation2024
IL-13 induces loss of CFTR in ionocytes and reduces airway epithelial fluid absorption.
Article in The Journal of clinical investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Understanding Nasal Polyposis: The Roles of Ion Channels, Inflammation, Ionocytes, and Prostaglandin E2-The IJournal of clinical medicine · 2026Article
- Coordinated immune-epithelial dynamics in the nasal epithelium protect against respiratory virus infection.bioRxiv : the preprint server for biology · 2026Article
- Considerations for early life genetic therapies in cystic fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2026Review
- Exposing the Airway Surface to the Neonicotinoid Clothianidin Alters the Electrophysiological Properties of Human Airway Epithelia.ACS omega · 2026Article
- Next Decade Research in Asthma: Broad Omics-Based Exploration Versus Targeted Airway Epithelium Studies.Journal of clinical medicine · 2025Review
- Genetically engineered approaches to the treatment of cystic fibrosis.Biophysical reviews · 2025Review
- Pulmonary Ionocytes at the Crossroads of Absorption and Secretion: Clues from the Ferret.American journal of respiratory and critical care medicine · 2025Article
- A translational view of airway epithelial dysfunction in COPD.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Ionocyte CFTR Coordinates Chloride Absorption and Secretion to Balance Airway Fluid.American journal of respiratory and critical care medicine · 2025Article
- Targeting IL-4/IL-13 Signaling Pathways in Chronic Rhinosinusitis with Nasal Polyps: From Mechanisms to Therapies.Clinical reviews in allergy & immunology · 2025Review
- Single cell profiling of human airway identifies tuft-ionocyte progenitor cells displaying cytokine-dependent differentiation bias in vitro.Nature communications · 2025Article
- The apical mucus layer alters the pharmacological properties of the airway epithelium.The Journal of physiology · 2025Article
- Comprehensive single-cell RNA-sequencing study of Tollip deficiency effect in IL-13-stimulated human airway epithelial cells.BMC research notes · 2025Article
- Innate Immunity and Asthma Exacerbations: Insights From Human Models.Immunological reviews · 2025Review
- Developmental immune network of airway lymphocytes and innate immune cells in patients with stable COPD.Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
The airway surface liquid (ASL) plays a crucial role in lung defense mechanisms, and its composition and volume are regulated by the airway epithelium. The cystic fibrosis transmembrane conductance regulator (CFTR) is abundantly expressed in a rare airway epithelial cell type called an ionocyte. Recently, we demonstrated that ionocytes can increase liquid absorption through apical CFTR and basolateral barttin/chloride channels, while airway secretory cells mediate liquid secretion through apical CFTR channels and basolateral NKCC1 transporters. Th2-driven (IL-4/IL-13) airway diseases, such as asthma, cause goblet cell metaplasia, accompanied by increased mucus production and airway secretions. In this study, we investigate the effect of IL-13 on chloride and liquid transport performed by ionocytes. IL-13 treatment of human airway epithelia was associated with reduced epithelial liquid absorption rates and increased ASL volume. Additionally, IL-13 treatment reduced the abundance of CFTR-positive ionocytes and increased the abundance of CFTR-positive secretory cells. Increasing ionocyte abundance attenuated liquid secretion caused by IL-13. Finally, CFTR-positive ionocytes were less common in asthma and chronic obstructive pulmonary disease and were associated with airflow obstruction. Our findings suggest that loss of CFTR in ionocytes contributes to the liquid secretion observed in IL-13-mediated airway diseases.
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