ArticleAmerican journal of respiratory cell and molecular biology2016
Rhinovirus Delays Cell Repolarization in a Model of Injured/Regenerating Human Airway Epithelium.
Article in American journal of respiratory cell and molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 42 citations in OpenAlex.
- Single-cell disentangled representations for perturbation modeling and treatment effect estimation.bioRxiv : the preprint server for biology · 2026Article
- The long reach of influenza and other respiratory viruses: from acute epithelial injury to post-viral lung disease.Clinical microbiology reviews · 2025Review
- Neuroinflammatory Consequences of Rhinovirus Infection in Human Epithelial and Neuronal Models.Lung · 2025Article
- Article
- HOXA1 Contributes to Bronchial Epithelial Cell Cycle Progression by Regulating p21/CDKN1A.International journal of molecular sciences · 2025Article
- Protective effect of interferon type I on barrier function of human airway epithelium during rhinovirus infections in vitro.Scientific reports · 2024Article
- Quercetin improves epithelial regeneration from airway basal cells of COPD patients.Respiratory research · 2024Article
- Rhinovirus induces airway remodeling: what are the physiological consequences?Respiratory research · 2023Review
- Airway Epithelial Cell Junctions as Targets for Pathogens and Antimicrobial Therapy.Pharmaceutics · 2022Review
- Airway tight junctions as targets of viral infections.Tissue barriers · 2021Article
- Up-Regulated Vitamin D Receptor byPharmaceuticals (Basel, Switzerland) · 2021Article
- E-Cadherin: An Important Functional Molecule at Respiratory Barrier Between Defence and Dysfunction.Frontiers in physiology · 2021Review
- Microarray analysis identifies defects in regenerative and immune response pathways in COPD airway basal cells.ERJ open research · 2020Article
- Nontypeable Haemophilus influenzae Responds to Virus-Infected Cells with a Significant Increase in Type IV Pilus Expression.mSphere · 2020Article
- Interleukin-13 Alters Tight Junction Proteins Expression Thereby Compromising Barrier Function and Dampens Rhinovirus Induced Immune Responses in Nasal Epithelium.Frontiers in cell and developmental biology · 2020Article
- Rhinovirus and Innate Immune Function of Airway Epithelium.Frontiers in cellular and infection microbiology · 2020Review
- More Than Just a Barrier: The Immune Functions of the Airway Epithelium in Asthma Pathogenesis.Frontiers in immunology · 2020Review
- Rhinovirus-Induced SIRT-1 via TLR2 Regulates Subsequent Type I and Type III IFN Responses in Airway Epithelial Cells.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Article
- Acute Respiratory Barrier Disruption by Ozone Exposure in Mice.Frontiers in immunology · 2019Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Rhinovirus (RV), which causes exacerbation in patients with chronic airway diseases, readily infects injured airway epithelium and has been reported to delay wound closure. In this study, we examined the effects of RV on cell repolarization and differentiation in a model of injured/regenerating airway epithelium (polarized, undifferentiated cells). RV causes only a transient barrier disruption in a model of normal (mucociliary-differentiated) airway epithelium. However, in the injury/regeneration model, RV prolongs barrier dysfunction and alters the differentiation of cells. The prolonged barrier dysfunction caused by RV was not a result of excessive cell death but was instead associated with epithelial-to-mesenchymal transition (EMT)-like features, such as reduced expression of the apicolateral junction and polarity complex proteins, E-cadherin, occludin, ZO-1, claudins 1 and 4, and Crumbs3 and increased expression of vimentin, a mesenchymal cell marker. The expression of Snail, a transcriptional repressor of tight and adherence junctions, was also up-regulated in RV-infected injured/regenerating airway epithelium, and inhibition of Snail reversed RV-induced EMT-like features. In addition, compared with sham-infected cells, the RV-infected injured/regenerating airway epithelium showed more goblet cells and fewer ciliated cells. Inhibition of epithelial growth factor receptor promoted repolarization of cells by inhibiting Snail and enhancing expression of E-cadherin, occludin, and Crumbs3 proteins, reduced the number of goblet cells, and increased the number of ciliated cells. Together, these results suggest that RV not only disrupts barrier function, but also interferes with normal renewal of injured/regenerating airway epithelium by inducing EMT-like features and subsequent goblet cell hyperplasia.
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