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Rhinoviruses and enterovirus-D68 replicate more robustly in respiratory tissues originating from asthmatic patients compared to non-asthmatic controls

ABSTRACT: Investigation of the mechanism leading to differential rhinovirus infection in airway epithelia from healty versus asthmatic patients

ORGANISM(S): Homo sapiens

PROVIDER: GSE222129 | GEO | 2023/02/13

REPOSITORIES: GEO

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Rhinoviruses and enterovirus-D68 replicate more robustly in respiratory tissues originating from asthmatic patients compared to non-asthmatic controls

Project description:Rhinoviruses and enterovirus-D68 replicate more robustly in respiratory tissues originating from asthmatic patients compared to non-asthmatic controls

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Phenotypic responses of differentiated asthmatic human airway epithelial cultures to rhinovirus

Project description:We report the application of RNA sequencing technology for high-throughput profiling of gene expression responses to human rhinovirus infection at 24 hours in air-liquid interface human airway epithelial cell cultures derived from 6 asthmatic and 6 non-asthmatic donors. RNA-seq analysis identified sets of genes associated with asthma specific viral responses. These genes are related to inflammatory pathways, epithelial remodeling and cilium assembly and function, including those described previously (e.g. CCL5, CXCL10 and CX3CL1), and novel ones that were identified for the first time in this study (e.g. CCRL1, CDHR3). We concluded that air liquid interface cultured human airway epithelial cells challenged with live HRV are a useful in vitro model for the study of rhinovirus induced asthma exacerbation, given that our findings are consistent with clinical data sets. Furthermore, our data suggest that abnormal airway epithelial structure and inflammatory signaling are important contributors to viral induced asthma exacerbation. Differentiated air-liquid interface cultured human airway epithelial cell mRNA profiles from 6 asthmatic and 6 non-asthmatic donors after 24 hour treatment with either HRV or vehicle control were generated by deep sequencing, using Illumina HiSeq 2000.

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Project description:Background: Evidence suggests that immune responses to rhinovirus A and C are altered in asthmatic children and rhinovirus species induce different types of antibody responses. Objective: To ascertain and compare the T-cell memory response induced by RV-A and RV-C in asthmatic and non-asthmatic children. Methods: Peripheral blood mononuclear cells from children who previously suffered asthma exacerbation (asthmatics) and non-asthmatic controls were stimulated in vitro with peptide formulations to induce representative species-specific responses to RV-A and RV-C. Expression of genes was measured by RNA-seq and differentially expressed genes were further analysed to identify enriched pathways and upstream regulators. Results: Responses to RV-A showed markedly higher upregulation of IFNG and the IFNG responsive genes CXCL9, 10 and 11 and STAT1 compared to RV-C. There was no reciprocal upregulation of Th2 cytokine genes or the Th2 chemokine genes CCL11, CCL17 and CCL22. RV-C but not RV-A induced high upregulation of CCL24 (eotaxin-2) in both non-asthmatic and asthmatic responses. Upstream regulator analysis showed both RV-A and, although to a diminished extent, RV-C induced predominant Th1 and inflammatory cytokine expression. The responses of asthmatics compared to non-asthmatics was diminished to both RV-A and RV-C while retaining the pattern for gene expression and upstream regulators characteristic of each species and there was no upregulation of Th2-type responses. All groups showed activation of the IL-17A pathway. Conclusions: RV-C induced memory cells with a lower IFNG type response than RV-A without Th2 upregulation. Asthmatics had lower recall responses than non-asthmatics while largely retaining the same gene activation profile for each species.

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