Ontology highlight
ABSTRACT:
PROVIDER: PRJNA544825 | ENA |
REPOSITORIES: ENA
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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
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. Thus, we hypothesis that asthmatic BSM cell metabolism is modified compare to that of non-asthmatic and that could be a potential target to reduce asthmatic BSM cell proliferation and remodeling in asthma.
2021-06-10 | PXD015566 | Pride
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
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.
2015-03-01 | GSE61141 | GEO
Project description:Murine Pulmonary Responses to Ambient Baltimore Particulate Matter: Genomic Analysis and Contribution to Airway Hyperresponsiveness; Asthma is a complex disease characterized by airway hyperresponsiveness (AHR) and chronic airway inflammation. Environmental factors such as ambient particulate matter (PM), a major air pollutant, has been demonstrated in epidemiological studies to contribute to asthma exacerbation and increased asthma prevalence. OBJECTIVE: We investigated the genomic and pathophysiological effects of Baltimore PM (median diameter 1.78 µm) in a murine model of asthma to identify potential biomarkers. METHODS: A/J mice with ovalbumin (OVA) âinduced AHR were exposed to PM (20 mg/kg, intratracheal), and both AHR and bronchoalveolar lavage (BAL) were assayed on days 1, 4, and 7 post exposure. Lung gene expression profiling (Affymetrix Mouse430_ 2.0) by PM (20 mg/kg, intratracheal) were assayed on OVA- and / or PM--challenged mice. RESULTS: Significant increases of airway responsiveness in OVA-treated mice were observed, indicating an asthmatic phenotype. Ambient PM exposure induced significant changes in AHR in both naive mice and OVA-induced asthmatic mice. In both naive and OVA challenged asthmatic mice, PM induced eosinophil and neutrophil infiltration into airways, elevated BAL protein content, and stimulated secretion of TH1 cytokines (IFN-g, IL-6, and TNF-a) and TH2 cytokines (IL-4, IL-5, and eotaxin) into BAL. Consistent with these results, PM induced expression of genes of innate immune response, chemotaxis and complementary system. CONCLUSION: These studies, consistent with epidemiological data, indicate that PM increases AHR and lung inflammation in naïve mice and exacerbates the asthma phenotype of increased AHR and gene expression pattern changes correlated with acute lung inflammation and airway damage. We used microarrays to detail the global programme of gene expression induced by rhPBEF treatment and VALI. Experiment Overall Design: animals were treated by PBS, Oval albumin, PM, or both OVA/PM
2008-06-16 | E-GEOD-9465 | biostudies-arrayexpress
Project description:A large, prospective, non-interventional study was designed to study gene expression changes in peripheral blood mononuclear cells (PBMCs) associated with asthma exacerbations over the course of a year. PBMC samples were collected from subjects at the time of the study visits defined as 1) Quiet: during stable disease at 3 month intervals, 2) Exacerbation: during a 14 day period of deteriorating asthma and 3) Follow-up: within 14 days after cessation of an exacerbation. Gene expression levels during stable asthma, exacerbation, and two weeks after an exacerbation were compared. This series of samples comprises of peripheral blood mononuclear cells (PBMCs) collected during the following study visits (a) quiet (N=394 samples from 118 subjects), (b) exacerbation (N=166 samples from 118 subjects) and (c) follow-up (N=125 samples from 102 subjects)
2011-07-13 | E-GEOD-19301 | biostudies-arrayexpress
Project description:A large, prospective, non-interventional study was designed to study gene expression changes in peripheral blood mononuclear cells (PBMCs) associated with asthma exacerbations over the course of a year. PBMC samples were collected from subjects at the time of the study visits defined as 1) Quiet: during stable disease at 3 month intervals, 2) Exacerbation: during a 14 day period of deteriorating asthma and 3) Follow-up: within 14 days after cessation of an exacerbation. Gene expression levels during stable asthma, exacerbation, and two weeks after an exacerbation were compared.
2011-07-14 | GSE19301 | GEO
Project description:Diesel exhaust particles (DEPs) are the main component of traffic-related air pollution and implicated in asthma pathogenesis and exacerbation. However, the mechanistic link between DEP exposure and worsening asthma symptoms remains unclear. Here, we characterized a unique subset of neutrophils that express a high level of Sialic acid-binding, Ig-like lectin (Siglec)-F. DEP exposure instructs SiglecF expression on neutrophils by increasing P2X1 receptors sensing damage-associated molecular patterns (DAMPs) molecules, ATP. SiglecFhigh neutrophils stimulated by DEP release neutrophil extracellular traps (NETs) to cause tissue damage and IL-17A production, and potentiated type 2 cytokine production by producing cysteinyl leukotrienes. As a result, SiglecFhigh neutrophils worsen airway hyperresponsiveness (AHR) as well as airway inflammations. We also confirmed that siglec8, corresponding to murine SiglecF, expression increased in neutrophils from patients with asthma, and they correlated with the severity of the disease. Together, these translational findings suggest a novel SiglecF expressing neutrophils in the development of severe asthma by linking type 2 and type 3 responses.
2022-09-01 | GSE158040 | GEO
Project description:Distinct Nasal Airway Bacterial Microbiota Differentially Relate to Exacerbation in Pediatric Asthma
| PRJEB25616 | ENA
Project description:To investigate mechanisms underlying frequent asthma exacerbation, we profiled the nasal transcriptome of both frequent and non-frequent asthma exacerbators.
2023-10-17 | GSE211158 | GEO