ArticleThe Journal of allergy and clinical immunology2024
Cholinergic sensing of allergen exposure by airway epithelium promotes type 2 immunity in the lungs.
Article in The Journal of allergy and clinical immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 8 citations in OpenAlex.
- Redox-sensitive GPCR signaling drives Gq-dependent CaAmerican journal of physiology. Cell physiology · 2026Article
- A novel mouse model of chronic Pseudomonas aeruginosa infection inducing bronchiectasis-like phenotype.Animal models and experimental medicine · 2026Article
- Interleukin-33 at the intersection of inflammation and repair.Frontiers in allergy · 2026Review
- The role of calcium homeostasis dysregulation in allergic rhinitis.Frontiers in immunology · 2026Review
- Chinese expert consensus on intranasal anticholinergics for allergic rhinitis.Asia Pacific allergy · 2025Review
- The Roles of Acetylcholine and Muscarinic Receptors in Allergic Rhinitis: Mechanisms, Clinical Insights and Future Directions.Current allergy and asthma reports · 2025Review
- The immunology of asthma and chronic rhinosinusitis.Nature reviews. Immunology · 2025Review
- Allergen-induced activation of epithelial P2YThe Journal of allergy and clinical immunology · 2025Article
- Targeting alarmins in asthma: From bench to clinic.The Journal of allergy and clinical immunology · 2025Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundNonneuronal cells, including epithelial cells, can produce acetylcholine (ACh). Muscarinic ACh receptor antagonists are used clinically to treat asthma and other medical conditions; however, knowledge regarding the roles of ACh in type 2 immunity is limited.
objectiveOur aim was to investigate the roles of epithelial ACh in allergic immune responses.
methodsHuman bronchial epithelial (HBE) cells were cultured with allergen extracts, and their ACh production and IL-33 secretion were studied in vitro. To investigate immune responses in vivo, naive BALB/c mice were treated intranasally with different muscarinic ACh receptor antagonists and then exposed intranasally to allergens.
resultsAt steady state, HBE cells expressed cellular components necessary for ACh production, including choline acetyltransferase and organic cation transporters. Exposure to allergens caused HBE cells to rapidly release ACh into the extracellular medium. Pharmacologic or small-interfering RNA-based blocking of ACh production or autocrine action through the M3 muscarinic ACh receptors in HBE cells suppressed allergen-induced ATP release, calcium mobilization, and extracellular secretion of IL-33. When naive mice were exposed to allergens, ACh was quickly released into the airway lumen. A series of clinical M3 muscarinic ACh receptor antagonists inhibited allergen-induced IL-33 secretion and innate type 2 immune response in the mouse airways. In a preclinical murine model of asthma, an ACh receptor antagonist suppressed allergen-induced airway inflammation and airway hyperreactivity.
conclusionsACh is released quickly by airway epithelial cells on allergen exposure, and it plays an important role in type 2 immunity. The epithelial ACh system can be considered a therapeutic target in allergic airway diseases.
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