ArticleScientific reports2021
Remodeling of bronchial epithelium caused by asthmatic inflammation affects its response to rhinovirus infection.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- A territory-wide study on adults hospitalized for rhinovirus infection - mortality, severe adverse respiratory and renal outcomes and relationships with multiple comorbidities.Journal of medical microbiology · 2026Article
- The role of virus in nasal inflammation.European journal of medical research · 2025Review
- IL-13 Modulates Antiviral Effector and Proinflammatory Pathways in Rhinovirus-Infected Pediatric Bronchial Epithelium.bioRxiv : the preprint server for biology · 2025Article
- CF airway epithelia display exaggerated host defense responses and prolonged cilia loss during RSV infection.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2025Article
- Bronchial smooth muscle extracellular vesicles interfere with bronchial epithelium metabolism and function in asthma.iScience · 2025Article
- Targeting Non-Eosinophilic Immunological Pathways in COPD and AECOPD: Current Insights and Therapeutic Strategies.International journal of chronic obstructive pulmonary disease · 2025Review
- Interleukin 13-Induced Inflammation Increases DPP4 Abundance but Does Not Enhance Middle East Respiratory Syndrome Coronavirus Replication in Airway Epithelia.The Journal of infectious diseases · 2024Article
- Tumor necrosis factor receptor-associated factor 5 enhances perianal fistulizing Crohn's disease through epithelial-mesenchymal transition.CytoJournal · 2024Article
- Interferon-independent processes constrain measles virus cell-to-cell spread in primary human airway epithelial cells.Microbiology spectrum · 2023Article
- Rhinovirus induces airway remodeling: what are the physiological consequences?Respiratory research · 2023Review
- Ιnterleukin-17A-Enriched Neutrophil Extracellular Traps Promote Immunofibrotic Aspects of Childhood Asthma Exacerbation.Biomedicines · 2023Article
- EPsInternational journal of molecular sciences · 2023Article
- Rhinovirus-induced epithelial RIG-I inflammasome suppresses antiviral immunity and promotes inflammation in asthma and COVID-19.Nature communications · 2023Article
- Regulation of angiotensin-converting enzyme 2 isoforms by type 2 inflammation and viral infection in human airway epithelium.Mucosal immunology · 2023Article
- Trained immunity in type 2 immune responses.Mucosal immunology · 2022Review
- Innate Immune Responses by Respiratory Viruses, Including Rhinovirus, During Asthma Exacerbation.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human rhinoviruses (HRV) are frequent cause of asthma exacerbations, however the influence of airway inflammation on the severity of viral infection is poorly understood. Here, we investigated how cytokine-induced remodeling of airway epithelium modulates antiviral response. We analyzed gene expression response in in vitro differentiated bronchial epithelium exposed to cytokines and next infected with HRV16. IL-13-induced mucous cell metaplasia (MCM) was associated with impaired ciliogenesis and induction of antiviral genes, resulting in lower susceptibility to HRV. Epithelial-mesenchymal transition caused by TGF-β was associated with increased virus replication and boosted innate response. Moreover, HRV infection per se caused transient upregulation of MCM markers and growth factors, followed by low-level virus replication and shedding. Our data suggest that the outcome of HRV infection depends on the type of lower airway inflammation and the extent of epithelial damage. Type-2 inflammation (eosinophilic asthma) may induce antiviral state of epithelium and decrease virus sensitivity, while growth factor exposure during epithelial repair may facilitate virus replication and inflammatory response. Additionally, responses to HRV were similar in cells obtained from asthma patients and control subjects, which implicates that antiviral mechanisms are not intrinsically impaired in asthma, but may develop in the presence of uncontrolled airway inflammation.
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