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DNA methylation in lung cells is a key modulator of asthma endotypes and genetic risk [RNA-seq]

ABSTRACT: We generated genome-wide RNASeq data from freshly isolated airway epithelial cells of asthmatics and non-asthmatics. This data was paired with genome-wide genetic and methylation data from the same individuals allowing for an integrated analysis of genetic, transcriptional, and epigenetic signatures in asthma.

ORGANISM(S): Homo sapiens

PROVIDER: GSE85567 | GEO | 2017/01/06

SECONDARY ACCESSION(S): PRJNA338808

REPOSITORIES: GEO

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DNA methylation in lung cells is a key modulator of asthma endotypes and genetic risk [DNA methylation]

Project description:We generated genome-wide methylation data using the 450K from freshly isolated airway epithelial cells of asthmatics and non-asthmatics. This data was paired with genome-wide genetic and gene expression data from the same individuals allowing for an integrated analysis of genetic, transcriptional, and epigenetic signatures in asthma.

2017-01-06 | GSE85566 | GEO

Lung function, airway and peripheral basophils and eosinophils are associated with molecular pharmacogenomic endotypes of steroid response in severe asthma.

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Network Dynamics of the Immune System decodes Asthma Endotypes

Project description:The ‘Genetic Epidemiology of Asthma in Costa Rica’ is a family-based cross-sectional cohort ascertained between February 2001 and August 2008 on a Hispanic population isolate from the Central Valley of Costa Rica. The study recruited children between 6 to 14 years of age with moderate persistent asthma.

2022-05-21 | GSE203482 | GEO

Identification of differences in CD4+ T-cell gene expression between people with asthma and healthy controls

Project description:Background: Functional enrichment analysis of genome-wide association study (GWAS)-summary statistics has suggested that immune cell-types, and especially CD4+ T-cells, play an important role in asthma pathogenesis. Despite this, CD4+ T-cells are under-represented in asthma transcriptome studies. Objective: To identify differences in gene expression between asthmatics and healthy controls in CD4+ T-cells. Methods: CD4+ T-cells were isolated within 2 hours from collection from peripheral blood from people with well-established asthma (n=33) and healthy controls (n=12). 3'-RNA-Seq was used to generate gene expression data. Weighted Gene Co-expression Network Analysis (WGCNA) was used to identify sets of co-expressed genes (modules). The asthma-associated modules were tested for enrichment of GWAS-identified asthma genes and gene ontology (GO) biological processes. For the genes in the asthma-associated modules, integration of eQTL and GWAS summary statistics (colocalisation), and protein-protein interaction (PPI) data was used to identify master regulators. Results: After quality control, 43 samples were available for the analysis. WGCNA identified three modules associated with asthma, which are strongly enriched for GWAS-identified asthma genes, antigen processing/presentation and immune response to viral infections. Colocalisation analysis of eQTL and GWAS summary statistics, together with PPI data, identified PTPRC as a master regulator of asthma gene-expression profiles in CD4+ T-cells. Conclusion: Unstimulated CD4+ T-cells from peripheral blood from asthmatics have different expression profiles, compared to healthy controls, for sets of genes involved in immune response to viral infections and antigen processing/presentation . Integration of genetic and protein-protein interaction data identified PTPRC as a master regulator of genes in asthma.

2023-12-27 | GSE217904 | GEO

DNA methylation in lung cells is a key modulator of asthma endotypes and genetic risk

Project description:DNA methylation in lung cells is a key modulator of asthma endotypes and genetic risk

| PRJNA338804 | ENA

Asthma Bronchial Biopsy Gene Expression

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

Systemic inflammation is associated with differential gene expression and airway neutrophilia in asthma

Project description:Systemic inflammation is reported to be associated with neutrophilic airway inflammation in asthma, this study aimed to examine the molecular mechanisms of the neutrophilia that is associated with systemic inflammation, and hypothesized that asthma patients with systemic inflammation have a group of genes that are differentially expressed and are assciated with airway inflammation. 50 asthma patients were recruited and grouped as asthmatics with systemic inflammation (n=18) and asthamtics without systemic inflammation (n=16) accroding to the levels of serum CRP and IL-6. RNA was extracted from induced sputum and was reverse-transcribed into cDNA. Gene profiling was performed using Illumina Sentrix HumanRef-8 Version 2 Expression BeadChips, and genes that were differentially expressed between asthmatics with systemic inflammation and asthmatics without systemic inflammation were compared and valided using qPCR.

2016-07-03 | E-GEOD-43397 | biostudies-arrayexpress

Novel mediators of eicosanoid and epithelial nitric oxide production in asthma

Project description:Asthma is a heterogeneous disease. Exercise-induced bronchoconstriction (EIB) is a distinct syndrome that occurs in 30-50% of asthmatics and is characterized by high levels of pro-inflammatory eicosanoids. We identified genes differentially expressed in the airways of asthmatics with EIB relative to asthmatics without EIB. Genes related to epithelial repair and mast cell infiltration including beta-tryptase and carboxypeptidase A3 were upregulated by exercise challenge in the asthma group with EIB. We confirmed that two novel mediators trefoil factor 3 (TFF3) and transglutaminase 2 (TGM2) have increased expression in airways cells and secreted product in the airways. In vitro studies indicate that 1) TFF3 induces nitric oxide synthase in airway epithelial cells from asthmatics and 2) TGM2 augments the enzymatic activity of secreted phospholipase A2 (sPLA2) group X, an enzyme recently been implicated in asthma pathogenesis. Since PLA2 serves as the first rate-limiting step leading to eicosanoid generation, these results suggest that TGM2 may be a key initiator of the airway inflammatory cascade in asthma.

2010-11-10 | GSE13785 | GEO

Airway epithelial gene expression in asthma versus healthy controls

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

Genome-wide profiling of an enhancer-associated histone modification reveals the influence of asthma on the epigenome of the airway epithelium.

Project description:Asthma is a chronic inflammatory disease of the airways driven by complex genetic-environmental interactions. Epigenomic mechanisms including histone modifications and DNA methylation are altered in key cell types of asthma. However, genome-wide studies of histone modifications in the airway epithelium of asthmatics have yet to be undertaken. We undertook genome-wide profiling of an enhancer (regulatory domain)-associated histone modification H3K27ac in bronchial epithelial cells (BECs) from asthmatic and healthy control individuals. We identified 49,903 (P<0.05) regions exhibiting differential H3K27ac enrichment in asthma and found they clustered predominately at genes associated with Th2-high asthma (e.g. CLCA1) and epithelial processes (e.g. EMT). We determined asthma had a dramatic influence on the enhancer landscape of BECs and identified asthma-associated Super-Enhancers encompassing genes encoding transcription factors (e.g. TP63) and enzymes involved in lipid metabolism (e.g. NOX4). We integrated published protein expression, epigenomic and transcriptomic datasets and identified epithelium-specific transcription factors associated with H3K27ac in asthma (e.g. TP73) and dynamic relationships between asthma-associated changes in H3K27ac, DNA methylation, genetic susceptibility and transcriptional profiles. Finally, using a CRISPR-based approach to recapitulate the H3K27ac landscape of asthma in vitro, we provide proof of principal that asthma-associated gene expression (e.g. SERPINB2) is driven in part by aberrant histone acetylation. This report identifies the influence of asthma on the epigenome of airway epithelium and provides evidence that aberrant epigenomic mechanisms exert functional consequences in key cell types of asthma, validating the combination of genome-wide and epigenome-editing approaches in identifying and deciphering the molecular mechanisms underlying asthma pathogenesis.

2019-06-04 | GSE109894 | GEO

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