ArticleThe Journal of allergy and clinical immunology2023
Rhinovirus infection of the airway epithelium enhances mast cell immune responses via epithelial-derived interferons.
Article in The Journal of allergy and clinical immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- Distinct epithelial and antiviral airway states in pediatric refractory asthma and rhinovirus-associated exacerbation.Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2026Article
- Article
- Neutrophilic asthma: advances in experimental models from pathogenesis to therapeutic translation.Molecular medicine (Cambridge, Mass.) · 2026Review
- The rhinovirus puzzle: Linking virus and host factors to childhood asthma.The Journal of allergy and clinical immunology · 2026Review
- IL-13 Modulates Antiviral Effector and Proinflammatory Pathways in Rhinovirus-Infected Pediatric Bronchial Epithelium.bioRxiv : the preprint server for biology · 2025Article
- Crosstalk between airway epithelial cells and mast cells in airway inflammation.Respiratory research · 2025Review
- The immunology of asthma.Nature immunology · 2025Review
- Innate Immunity and Asthma Exacerbations: Insights From Human Models.Immunological reviews · 2025Review
- Toll-like receptor activation induces airway obstruction and hyperresponsiveness in guinea pigs.Respiratory research · 2024Article
- Advances in non-type 2 severe asthma: from molecular insights to novel treatment strategies.The European respiratory journal · 2024Review
- Wnt5a-mediated autophagy contributes to the epithelial-mesenchymal transition of human bronchial epithelial cells during asthma.Molecular medicine (Cambridge, Mass.) · 2024Article
- A Fast Scoring of Human Primary Respiratory Epithelia Grown at Air-Liquid Interface (ALI) to Assess Epithelial Morphology in Research and Personalized Medicine Settings.Journal of personalized medicine · 2024Article
- Distinct Epithelial-Innate Immune Cell Transcriptional Circuits Underlie Airway Hyperresponsiveness in Asthma.American journal of respiratory and critical care medicine · 2023Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundMast cells (MCs) within the airway epithelium in asthma are closely related to airway dysfunction, but cross talk between airway epithelial cells (AECs) and MCs in asthma remains incompletely understood. Human rhinovirus (RV) infections are key triggers for asthma progression, and AECs from individuals with asthma may have dysregulated antiviral responses.
objectiveWe utilized primary AECs in an ex vivo coculture model system to examine cross talk between AECs and MCs after epithelial rhinovirus infection.
methodsPrimary AECs were obtained from 11 children with asthma and 10 healthy children, differentiated at air-liquid interface, and cultured in the presence of laboratory of allergic diseases 2 (LAD2) MCs. AECs were infected with rhinovirus serogroup A 16 (RV16) for 48 hours. RNA isolated from both AECs and MCs underwent RNA sequencing. Direct effects of epithelial-derived interferons on LAD2 MCs were examined by real-time quantitative PCR.
resultsMCs increased expression of proinflammatory and antiviral genes in AECs. AECs demonstrated a robust antiviral response after RV16 infection that resulted in significant changes in MC gene expression, including upregulation of genes involved in antiviral responses, leukocyte activation, and type 2 inflammation. Subsequent ex vivo modeling demonstrated that IFN-β induces MC type 2 gene expression. The effects of AEC donor phenotype were small relative to the effects of viral infection and the presence of MCs.
conclusionsThere is significant cross talk between AECs and MCs, which are present in the epithelium in asthma. Epithelial-derived interferons not only play a role in viral suppression but also further alter MC immune responses including specific type 2 genes.
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