1506_Methylation_M.vd.Berge
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ABSTRACT:
PROVIDER: EGAD00010001731 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:The study focus was differential methylation in bronchial biopsies between persistent asthma, asthma in remission and healthy controls using Illumina 450k arrays.
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Project description:We performed small RNA sequencing (TruSeq) of gene expression on bronchial cells from human bronchial epithelial brushings from 16 independent subjects whose samples were classified as either healthy controls (with no asthma or lung disease) or steroid-naive asthmatics (subjects with asthma not using inhaled corticosteroids (ICS) for 6 weeks before enrollment that were studied at baseline ('Steroid-naive asthma - Baseline') or after 8 weeks of treatment with budesonide, 200 μg twice a day, ('Steroid-naive asthma - Post-ICS treatment')). The goal was to assess abundance of miRNAs in all the samples collectively.
2021-01-01 | GSE164119 | GEO
Project description:Transcriptional profiling of lung bronchial biospsy mRNA from asthmatics Two-condition experiment, mRNA from asthma bronchial biopsies for test channel and Stratagene Universal Human Reference RNA for reference channel.
2015-09-08 | E-GEOD-69497 | biostudies-arrayexpress
Project description:To better understand the therapeutic potential of targeting Th2 inflammation in asthma, we performed genome-wide expression profiling of endobronchial biopsies in asthmatics and healthy controls stratified according a previously defined three-gene Th2 signature in bronchial epithelium. The Th2 signature is defined as relatively high expression of POSTN, CLCA1, and SERPINB2.
2011-01-18 | GSE23611 | GEO
Project description:The airway epithelium forms the interface between the inhaled environment and the lung. The airway epithelium is dysfunctional in asthma and epigenetic mechanisms are considered a contributory factor. We hypothesised that the DNA methylation profiles of cultured primary airway epithelial cells (AECs) would differ between cells isolated from individuals with asthma (n=17) versus those without asthma (n=16). AECs were isolated from patients by two different isolation techniques; pronase digestion (9 non-asthmatic, 8 asthmatic) and bronchial brushings (7 non-asthmatic and 9 asthmatic). DNA methylation was assessed using an Illumina Infinium HumanMethylation450 BeadChip array. DNA methylation of AECs clustered by isolation technique and linear regression identified 111 CpG sites differentially methylated between isolation techniques in healthy individuals. As a consequence, the effect of asthmatic status on DNA methylation was assessed within AEC samples isolated using the same technique. In pronase isolated AECs, 15 DNA regions were differentially methylated between asthmatics and non-asthmatics. In bronchial brush isolated AECs, 849 differentially methylated DNA regions were identified with no overlap to pronase regions. In conclusion, regardless of cell isolation technique, differential DNA methylation was associated with asthmatic status in AECs, providing further evidence for aberrant DNA methylation as a signature of epithelial dysfunction in asthma.
2019-10-31 | GSE137716 | GEO
Project description:Airway epithelial brushings were obtained for microarray analysis by research bronchoscopy in 62 subjects with mild-to-moderate asthma not on inhaled steroids and 43 healthy controls. Asthma subjects were stratified into 2 subgroups, Th2 high and Th2 low asthma, based on their expression of a three-gene signature of Type 2 inflammation: POSTN, SERPINB2, and CLCA1. Gene expression comparisons were made between: 1. asthmatics and healthy controls, and 2. Th2 high asthma and Th2 Low asthma/Healthy controls. The gene expression alterations most associated with asthma were then used in gene set enrichment analyses and gene signature development to compare this asthma dataset to COPD gene expression datasets.
2015-04-01 | E-GEOD-67472 | biostudies-arrayexpress
Project description:The study focus was differential expression in bronchial biopsies between persistent asthma, asthma in remission and healthy controls using RNAseq.
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Project description:Asthma pathogenesis and susceptibility involves a complex interplay between genetic and environmental factors. We report the results of expression microarray studies using tissue obtained from bronchial biopsies of healthy controls and of subjects with allergic asthma, both before and following inhaled corticotherapy.
2009-04-24 | GSE15823 | GEO
Project description:Molecular profiling studies in asthma cohorts have identified a Th2-driven asthma subtype, characterized by elevated lower airway expression of POSTN, CLCA1 and SERPINB2. To assess upper airway gene expression as a potential biomarker for lower airway Th2 inflammation, we assayed upper airway (nasal) and lower airway (bronchial) epithelial gene expression, serum total IgE, blood eosinophils and serum periostin in a cohort of 54 allergic asthmatics and 30 matched healthy controls. 23 of 51 asthmatics in our cohort were classified as âTh2 highâ based on lower airway Th2 gene signature expression. Consistent with this classification, âTh2 highâ subjects displayed elevated total IgE and blood eosinophil levels relative to âTh2 lowâ subjects. Upper airway Th2 signature expression was significantly correlated with lower airway Th2 signature expression (r=0.44), with similar strength of association as serum total IgE and blood eosinophils, known biomarkers of Th2 inflammation. In an unbiased genome-wide scan, we identified 8 upper airway genes more strongly correlated with lower airway Th2 gene signature expression (r=0.58), including Eotaxin-3 (CCL26), Galectin-10 (CLC) and Cathepsin-C (CTSC). Asthmatics classified as âTh2 highâ using this 8-gene signature show similar serum total IgE and blood eosinophil levels as âTh2 highâ asthmatics classified using lower airway Th2 gene signature expression. We have identified an 8-gene upper airway signature correlated with lower airway Th2 inflammation, which may be used as a diagnostic biomarker for Th2-driven asthma. Upper airway (nasal) and lower airway (bronchial) epithelial brushings obtained from a cohort of 54 allergic asthmatics and 30 matched healthy controls were profiled by gene expression by microarray. Subjects were assayed for gene expression, serum total IgE, blood eosinophils and serum periostin.
2015-10-23 | E-GEOD-41861 | biostudies-arrayexpress
Project description:Rationale: DNA methylation plays a critical role in asthma development, but differences in DNA methylation associated with asthma severity, especially among adults, are less well-defined. Changes in DNA methylation are influenced by exposure to air pollution, which is a risk factor for asthma exacerbation and severity. Here, we examined how DNA methylomic patterns in adult asthmatics differ by asthma severity and exposure to different components of air pollution. Methods: Peripheral blood CD3+ T cells from adult asthmatics in Beijing, China were serially collected from 37 patients (130 samples total) and analyzed for global DNA methylation using the Illumina MethylationEPIC Array. Measurements and Main Results: Significant differences in DNA methylation were noted among subjects with different degrees of asthma severity, as measured by fraction of exhaled nitric oxide, forced expiratory volume, and asthma control test scores. Differences in DNA methylation were annotated to genes that were enriched in pathways related to asthma or T cell function, and included gene ontology categories related to cellular adhesion, developmental pathways, and calcium signaling. Notable genes that were differentially methylated based on asthma severity included RUNX3, several members of the HLA family, PDGFRA, CDH1, CAV1, and NOTCH4. Differences in DNA methylation also varied by exposure to ambient air pollution, with different components of pollution effecting methylation of different groups of genes. Conclusion: These findings demonstrate how adult asthmatics possess widespread differences in the DNA methylation that associated with varying asthma severity and how air pollution might contribute to more severe asthma via changes in DNA methylation.
2024-07-31 | GSE226257 | GEO