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Differential gene expression of lymphocytes stimulated with rhinovirus species A and C in asthmatic and non-asthmatic children

ABSTRACT: Differential gene expression of lymphocytes stimulated with rhinovirus species A and C in asthmatic and non-asthmatic children

PROVIDER: PRJNA557698 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9874340.fastq.gz	Fastqsanger.gz
	SRR9874350.fastq.gz	Fastqsanger.gz
	SRR9874360.fastq.gz	Fastqsanger.gz
	SRR9874370.fastq.gz	Fastqsanger.gz
	SRR9874380.fastq.gz	Fastqsanger.gz

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Differential gene expression of lymphocytes stimulated with rhinovirus species A and C in asthmatic and non-asthmatic children

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.

2020-08-10 | GSE135192 | GEO

Severe asthmatic bronchial smooth muscle decreases epithelial response to rhinovirus infection.

Project description:Asthma is a very frequent airway disease that affects 6 to 20% of the population. Severe asthma, represents 3 to 5% of all asthmatic patients and is histologically characterized by an increased bronchial smooth muscle (BSM) mass and clinically by viral exacerbations. Functionally, BSM remodeling had a poor prognostic value in asthma, since higher BSM mass was associated with lower lung function and increased exacerbation rate. However, the role of BSM as a potential actor of asthma exacerbation has only been sparsely suggested. We thus hypothesis that asthmatic BSM cells could act on bronchial epithelium and modified its response to rhinovirus infection.

2023-05-02 | PXD015604 | Pride

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.

2015-03-01 | E-GEOD-61141 | biostudies-arrayexpress

Phenotypic responses of differentiated asthmatic human airway epithelial cultures to rhinovirus

2015-03-01 | GSE61141 | GEO

Breath Metabolites from Healthy and Asthmatic Children

Project description:mzML files used to generate Figure 1A-F, Figure S1D-E, Figure 7B, Figure S5A-F. Breath samples collected from healthy and asthmatic children

2024-07-15 | MSV000095340 | MassIVE

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

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

2023-02-13 | GSE222129 | GEO

Transcription profiling of human bronchial epithelial cells from normal and asthmatic subjects exposed to either ozone or rhinovirus

Project description:The exacerbation of disease in asthmatics has been linked to both exposure to environmental agents as well as to the presence of virus in airways, particularly rhinovirus. The hypothesis tested in these experiments is that differences in gene expression profiles in epithelial cells derived from asthmatic and normal airways can be linked to enhanced responsiveness of the epithelium in its pro-inflammatory, immulogic or other activities that may lead to the exacerbation of disease.

2007-12-12 | E-GEOD-470 | biostudies-arrayexpress

Human rhinovirus infection causes different DNA methylation changes in nasal epithelial cells from healthy and asthmatic subjects

Project description:Background: Mechanisms underlying the development of virus-induced asthma exacerbations remain unclear. Objective: To investigate if epigenetic mechanisms could be involved in virus-induced asthma exacerbations, we undertook DNA methylation profiling in asthmatic and healthy nasal epithelial cells (NECs) during Human Rhinovirus (HRV) infection in vitro. Methods: Global and loci-specific methylation profiles were determined via Alu element and Infinium Human Methylation 450K microarray respectively. Principal components analysis identified the genomic loci influenced the most by disease-status and infection. Real-time PCR and pyrosequencing was used to confirm gene expression and DNA methylation respectively. Results: Global methylation was increased in Asthmatics during infection. Disease status and virus infection influenced the methylation of 389 loci. Healthy and asthmatic NECs were characterized predominately by methylation profiles and patterns in loci that were not influenced by virus infection. However, both groups also exhibited distinct DNA methylation profiles in response to infection. Despite these differences, we found that the methylation of small nucleolar RNA, H/ACA box 12 (SNORA12) was common during infection. Further analysis indicated a relationship existed between SNORA12 DNA methylation and gene expression in response to infection. Conclusions: Findings from our study indicate that in addition to the well described phenotypic and genomic differences, the airway epithelium of asthmatics is characterized by a distinct methylome and that epigenetic mechanism may contribute to the development of virus-induced asthma exacerbations. Bisulphite converted DNA from matched mock and human rhinovirus-16 infected nasal epithelial cells from Healthy (n=3) and Asthmatics (n=6) adults were hybridized to the Illumina DNA methylation 450K Bead Array.

2014-07-28 | E-GEOD-52074 | biostudies-arrayexpress

Genome-wide analysis of whole blood transcriptional response to Respiratory Syncytial Virus, Influenza and Rhinovirus lower respiratory tract infection (LRTI) in children

Project description:Analysis of transcriptional profiles in whole blood from children < 2 years of age (and healthy matched controls) with RSV, rhinovirus and influenza infection. The hypothesis tested is that transcriptional profile heterogeneity will reflect patient clinical heterogeneity and that RSV infection induces a distinct host response compared with influenza and rhinovirus infection Total RNA extracted from whole blood (lysed in Tempus tubes) drawn from individual pediatric patients with acute RSV, influenza and Rhinovirus lower respiratory tract infection. A total of 241 samples are analyzed: 135 with acute RSV LRTI, 30 with Rhinovirus LRTI, 16 with influenza LRTI, 39 age-sex matched healthy controls and 21 samples obtained one month after the acute hospitalization in children with RSV. Samples GSM1226237-GSM1226272, which were hybridized to Platform GPL10558, were normalized separately from the other Samples in this Series, which were hybridized to Platform GPL6884. 'GSE38900_non-normalized_GSM1226237-GSM1226272.txt.gz' includes the non-normalized data for Samples GSM1226237-GSM1226272; 'GSE38900_non-normalized.txt.gz' includes the non-normalized data for the other Samples.

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Genome-wide analysis of whole blood transcriptional response to Respiratory Syncytial Virus, Influenza and Rhinovirus lower respiratory tract infection (LRTI) in children

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