ArticleAllergy2023
Epigenetic responses to rhinovirus exposure in airway epithelial cells are correlated with key transcriptional pathways in chronic rhinosinusitis.
Article in Allergy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The trial behind it
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Rhinovirus and interleukin-13 alter DNA methylation in bronchial epithelial cells at asthma loci.ERJ open research · 2026Article
- Unraveling the layers of epigenetic control in respiratory antiviral defense.Journal of virology · 2026Review
- Airway epithelial heterogeneity and mucus plugging in asthmatic bronchioles.American journal of respiratory and critical care medicine · 2026Article
- Uncovering the immune-related PCD genes in chronic rhinosinusitis with nasal polyps inflammatory progression: a machine learning and functional validation study.Frontiers in cell and developmental biology · 2026Article
- The role of virus in nasal inflammation.European journal of medical research · 2025Review
- Unveiling the prevalence and impact of silent rhinovirus infection in chronic rhinosinusitis with nasal polyps.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2025Article
- Epigenetic training of human bronchial epithelium cells by repeated rhinovirus infections.Allergy · 2024Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundViruses may drive immune mechanisms responsible for chronic rhinosinusitis with nasal polyposis (CRSwNP), but little is known about the underlying molecular mechanisms.
objectivesTo identify epigenetic and transcriptional responses to a common upper respiratory pathogen, rhinovirus (RV), that are specific to patients with CRSwNP using a primary sinonasal epithelial cell culture model.
methodsAirway epithelial cells were collected at surgery from patients with CRSwNP (cases) and from controls without sinus disease, cultured, and then exposed to RV or vehicle for 48 h. Differential gene expression and DNA methylation (DNAm) between cases and controls in response to RV were determined using linear mixed models. Weighted gene co-expression analysis (WGCNA) was used to identify (a) co-regulated gene expression and DNAm signatures, and (b) genes, pathways, and regulatory mechanisms specific to CRSwNP.
resultsWe identified 5585 differential transcriptional and 261 DNAm responses (FDR <0.10) to RV between CRSwNP cases and controls. These differential responses formed three co-expression/co-methylation modules that were related to CRSwNP and three that were related to RV (Bonferroni corrected p < .01). Most (95%) of the differentially methylated CpGs (DMCs) were in modules related to CRSwNP, whereas the differentially expressed genes (DEGs) were more equally distributed between the CRSwNP- and RV-related modules. Genes in the CRSwNP-related modules were enriched in known CRS and/or viral response immune pathways.
conclusionRV activates specific epigenetic programs and correlated transcriptional networks in the sinonasal epithelium of individuals with CRSwNP. These novel observations suggest epigenetic signatures specific to patients with CRSwNP modulate response to viral pathogens at the mucosal environmental interface. Determining how viral response pathways are involved in epithelial inflammation in CRSwNP could lead to therapeutic targets for this burdensome airway disorder.
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