Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Acute rhinovirus infection induces extensive antiviral and B cell receptor gene expression in B cells from asthmatics

ABSTRACT: B cells of asthmatic patients have dysregulated expression of inflammatory cytokine, B cell receptor and antiviral genes at a steady-state. During experimental in vivo infection of human subjects with rhinovirus, interferon-induced antiviral response is exaggerated in B cells in asthmatic patients.

ORGANISM(S): Homo sapiens

PROVIDER: GSE118875 | GEO | 2021/07/03

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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

Acute rhinovirus infection induces extensive antiviral and B cell receptor gene expression in B cells from asthmatics

Project description:Acute rhinovirus infection induces extensive antiviral and B cell receptor gene expression in B cells from asthmatics

| PRJNA487084 | ENA

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

Rhinovirus-induced modulation of gene expression in bronchial epithelial cells from subjects with asthma

Project description:Human Rhinovirus (HRV) infection can trigger exacerbations of asthma. Understanding of the mechanisms provoking airway inflammation and remodeling in asthma, as well as the pathogenic mechanisms of HRV infection and its association with asthma exacerbations, may offer significant opportunities for improved disease management. Genome-wide expression analysis of HRV type 1A-infected primary bronchial epithelial (PBE) cells from normal and asthmatic donors was performed to determine whether asthma is associated with a unique pattern of gene expression after HRV infection in vitro. Keywords: response to rhinovirus infection

2008-11-01 | GSE13396 | GEO

Phenotypic responses of differentiated asthmatic human airway epithelial cultures to rhinovirus

2015-03-01 | GSE61141 | GEO

Rhinovirus-induced epithelial RIG-I inflammasome suppresses antiviral immunity and promotes inflammation in asthma and COVID-19

Project description:Balanced immune responses in airways of patients with asthma are crucial to succesful clearance of viral infection and proper asthma control. We used microarrays to detail the global programme of gene expression data from bronchial brushings from control individuals and patients with asthma after rhinovirus infection in vivo.

2023-03-14 | GSE185658 | GEO

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

RNA-sequencing of bronchial epithelial cells from an adult cohort including asthmatics, COPD and healthy controls, cultured with Rhinovirus 1A

Project description:Rhinovirus infections exacerbate chronic respiratory inflammatory diseases such as asthma and chronic obstructive pulmonary disease (COPD). Airway epithelial cells are the primary site of rhinovirus replication and responsible for initiating the host immune response to infection. Numerous studies have reported that the anti-viral innate immune response in asthma is deficient leading to the conclusion that epithelial innate immunity is a key determinant of disease severity during a rhinovirus induced exacerbation. However, deficient rhinovirus-induced epithelial interferon production in asthma has not always been observed. We hypothesised that disparate in vitro airway epithelial infection models lacking genome-wide, time-course analyses have obscured the role of epithelial innate anti-viral immunity in asthma and COPD. To address this, we developed a low multiplicity of infection (MOI) rhinovirus model of differentiated primary epithelial cells obtained from healthy, asthma and COPD donors. Using genome-wide gene expression following infection, we demonstrated that gene expression patterns are similar across patient groups, but that the kinetics of induction are delayed in cells obtained from asthma and COPD donors. Rhinovirus-induced innate immune responses were defined by interferons (type-I, II and III), interferon response factors (IRF1, IRF3 and IRF7), TLR signalling and NF‐kB and STAT1 activation. Induced gene expression was evident at 24 hours and peaked at 48 hours post‐infection in cells from healthy subjects. In contrast, in cells from donors with asthma or COPD induction was maximal at or beyond 72-96 hours post infection. Thus, we propose that propensity for viral exacerbations of asthma and COPD relate to delayed (rather than deficient) expression of epithelial cell innate anti-viral immune genes which in turns leads to a delayed and ultimately more inflammatory host immune response.

2020-05-10 | GSE146532 | GEO

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

Rhinovirus infection results in stronger and more persistent genomic dysregulation: evidence for altered innate immune response in asthmatics at baseline, early in infection, and during convalescence

Project description:Background: Rhinovirus (HRV) is associated with the large majority of virus-induced asthma exacerbations in children and young adults, but the mechanisms remain poorly defined. Methods: Asthmatics and non-asthmatic controls were inoculated with HRV-A16, and nasal epithelial samples were obtained 7 days before, 36 hours after, and 7 days after viral inoculation. RNA was extracted and subjected to RNA-seq analysis. Results: At baseline, 57 genes were differentially expressed between asthmatics and controls, and the asthmatics had decreased expression of viral replication inhibitors and increased expression of genes involved in inflammation. At 36 hours (before the emergence of peak symptoms), 1329 genes were significantly altered from baseline in the asthmatics compared to 62 genes in the controls. At this time point, asthmatics lacked an increase in IL-10 signaling observed in the controls. At 7 days following HRV inoculation, 222 genes were significantly dysregulated in the asthmatics, whereas only 4 genes were dysregulated among controls. At this time point, the controls but not asthmatics demonstrated upregulation of SPINK5. Conclusions: As judged by the magnitude and persistence of dysregulated genes, asthmatics have a substantially different host response to HRV-A16 infection compared with non-asthmatic controls. Gene expression differences illuminate biologically plausible mechanisms that contribute to a better understanding of the pathogenesis of HRV-induced asthma exacerbations.

2017-05-26 | GSE97668 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data