ArticleMucosal immunology2025
Rhinovirus C15 infection induces airway epithelial cell remodeling and robust inflammatory responses: Potential implications for airway obstruction in children.
Article in Mucosal immunology, 2025. 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 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.
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Who cites it
5 citing papers in PubMed.
- Airway epithelia clear rhinovirus infection via two waves of cell extrusion.Science advances · 2026Article
- A robust cell-based infection model for Rhinovirus C research and antiviral drug discovery.Npj viruses · 2026Article
- Unique nasal cell states induced by common pediatric respiratory viruses.bioRxiv : the preprint server for biology · 2026Article
- The rhinovirus puzzle: Linking virus and host factors to childhood asthma.The Journal of allergy and clinical immunology · 2026Review
- Temporal Nasal Epithelial Gene Expression Patterns in Healthy Individuals Infected With Rhinovirus-16, and Its Modulation by Carrot Rhamnogalacturonan-I.Journal of medical virology · 2026Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Despite recognition of rhinovirus-C (RV-C) as a cause of severe respiratory exacerbations, little is known about the pathogenesis of RV-C infections. We infected mucociliary-differentiated primary tracheobronchial epithelial cells with RV-C15 or RV-A16. Initial RNASeq data showed that, compared to RV-A16, RV-C15 decreased expression of genes related to ciliary function while increasing expression of genes associated with mucus secretion and inflammation. Using different airway epithelial cell isolates, we confirmed greater reduction in DNAI2 and FOXJ1 (regulates production of motile cilia) and increased FOXA3 (regulates mucin -related gene expression) after RV-C15 infection compared to RV-A16. Similarly, nasal swab samples from children with RV-C but not RV-A infections showed significantly decreased DNAI2 and FOXJ1 mRNA compared to controls. While both RV-C15 and RV-A16 infection of airway epithelial cells increased mRNA expression and secretion of MUC5AC, RV-C15 induced greater airway surface liquid thickness, as measured by FITC-dextran staining. DAPT, a Notch inhibitor, reversed the effects of RV-C15 on DNAI2, FOXJ1 and FOXA3 expression. RV-C15 induced loss of α-acetyl tubulin, extrusion of airway epithelial cells, dissociation of ZO-1 from tight junctions, reduced ciliary beat frequency and decreased epithelial cell transepithelial electrical resistance. Finally, protein abundance of pro-inflammatory cytokines in cell supernatants and nasal samples also tended to be higher after RV-C infection. We conclude that RV-C causes significant disruptions in airway epithelial cell ciliary function which may lead to airway obstruction. Such disruptions may play a role in the severity of RV-C respiratory tract infections.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.