ArticleAllergy2026
Acetylcholine From Solitary Chemosensory Cell, Not Neuron, Regulates Basal Cell Fate Driving Eosinophilic Chronic Rhinosinusitis With Nasal Polyps.
Article in Allergy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
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Who cites it
2 citing papers in PubMed.
- Article
- The role of calcium homeostasis dysregulation in allergic rhinitis.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
21 authors.
Funding
Abstract
backgroundBasal cells (BCs) play a crucial role in epithelial remodeling, a hallmark of eosinophilic chronic rhinosinusitis with nasal polyps (eCRSwNP). Single-cell sequencing has revealed an increased number of solitary chemosensory cells (SCCs) alongside BC hyperplasia in eCRSwNP, yet the underlying mechanism of BC hyperplasia in eCRSwNP remains unclear. This study aimed to investigate the role of SCC-derived acetylcholine (Ach) in determining BC fate.
methodsTissue samples from healthy individuals, patients with eCRSwNP, and those with non-eCRSwNP (neCRSwNP) were analyzed to investigate BC proliferation, differentiation abnormalities, and the prevalence of SCCs. The relationship between SCC-derived Ach, BC dysfunction, and disease severity was examined. Ach sources and receptor expression patterns were characterized. In vitro studies using submerged cell cultures and air-liquid interface cultures, along with in vivo murine models, were employed to elucidate the mechanisms by which Ach influences BC fate. The inhibitory effects of tiotropium bromide (TB) on Ach-driven processes were also evaluated.
resultsOur results indicated that SCC-derived Ach, rather than by parasympathetic nerves, contributed to abnormal BC proliferation and differentiation through muscarinic acetylcholine receptors (mAChRs) and had potential impact on the development of eCRSwNP. These effects were associated with the activation of YAP and could be partially reversed both in vitro and in vivo by blocking mAChRs with TB.
conclusionThese results demonstrate that SCC-derived Ach plays a critical role in eCRSwNP by regulating BC fate. This provides a potential translational framework for developing prevention and treatment strategies targeting the cholinergic pathway.
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