Asthma Bronchial Biopsy Gene Expression
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: David Choy
PROVIDER: E-GEOD-69497 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Transcriptional profiling of lung bronchial biospsy mRNA from asthmatics
2015-09-08 | GSE69497 | GEO
Project description:Bronchial epithelial brushings were obtained by bronchoscopy from 8 steroid-naïve asthmatics including type 2-low (n=4) and type 2-high asthma (n=4), and 4 healthy controls. The type 2-low and –high asthma was defined by the epithelial expression of a three-gene signature for type 2 status (POSTN, SERPINB2, and CLCA1).
2019-12-18 | GSE142237 | 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:Asthma is a complex syndrome associated with episodic decompensations provoked by aeroaller-gen exposures. The underlying pathophysiological states driving exacerbations are latent in the resting state and do not adequately inform biomarker-driven therapy. A better understanding of the pathophysiological pathways driving allergic exacerbations is needed. We hypothesized that disease-associated pathways could be identified in humans by unbiased metabolomics of bron-choalveolar fluid (BALF) during the peak inflammatory response provoked by a bronchial aller-gen challenge. We analyzed BALF metabolites in samples from 12 volunteers who underwent segmental bronchial antigen provocation (SBP-Ag). Metabolites were quantified using liquid chromatography-tandem mass spectrometry (LC–MS/MS) followed by pathway analysis and cor-relation with airway inflammation. SBP-Ag induced statistically significant changes in 549 fea-tures that mapped to 72 uniquely identified metabolites. From these features, two distinct induci-ble metabolic phenotypes were identified by the principal component analysis, partitioning around medoids (PAM) and k-means clustering. Ten index metabolites were identified that in-formed the presence of asthma-relevant pathways, including unsaturated fatty acid produc-tion/metabolism, mitochondrial beta oxidation of unsaturated fatty acid, and bile acid metabolism. Pathways were validated using proteomics in eosinophils. A segmental bronchial allergen chal-lenge induces distinct metabolic responses in humans, providing insight into pathogenic and pro-tective endotypes in allergic asthma.
2022-06-09 | PXD033172 | Pride
Project description:Biological mechanisms explaining asthma control improvement following bronchial thermoplasty are still not well understood. We used a large-scale transcriptomic approach to evaluate the transcriptome of bronchial epithelial cell (BEC) obtained before and after bronchial thermoplasty treatment (BT).
2023-11-29 | GSE216617 | GEO
Project description:Via extensive comparative analysis of 3D human bronchial epithelial model (MucilAirTM) exposed to air or CuO-based aerosols, we show that existence of asthma enhances sensitivity of the airways to nanoparticles, possibly as a combined result of a hyperactive airway and inefficient mucociliary clearance mechanisms in asthmatics.
2019-05-01 | GSE127773 | GEO
Project description:Rationale: Augmented smooth muscle contractility of the airways is one of the causes of airway hyperresponsiveness in asthmatics. However, the mechanism of the altered properties of airway smooth muscle cells is not well understood. Objectives: To identify differentially expressed genes (DEGs) related to the bronchial smooth muscle (BSM) hyper-contractility in a murine asthma model. Methods: The ovalbumin (OA)-sensitized mice were repeatedly challenged with aerosolized OA to induce asthmatic reaction. Transcriptomic profiles were generated by microarray analysis of BSMs from the OA-challenged and control animals, and KEGG (Kyoto Encyclopedia of Genes and Genomes) Pathway Analysis was applied. Measurements and Main Results: Tension study showed a BSM hyperresponsiveness to acetylcholine (ACh) in the OA-challenged mice. A total of 770 genes were differentially expressed between the OA-challenged and control animals. Pathway analysis showed a significant change in arachidonic acid (AA) metabolism pathway in BSMs of the OA-challenged mice. Validation of DEGs by quantitative RT-PCR showed a significant increase in PLA2 group 4c (Pla2g4c)/COX-2 (Ptgs2)/PGD2 synthase 2 (Hpgds) axis. PGD2 level in bronchoalveolar fluids of the OA-challenged mice was significantly increased. A 24-h incubation of BSMs with PGD2 caused a hyperresponsiveness to ACh in naive control mice. Conclusions: AA metabolism is shifted towards PGD2 production in BSMs of asthma. Increased PGD2 level in the airways might be a cause of the BSM hyperresponsiveness in asthma.
2018-07-03 | GSE116504 | GEO
Project description:Bronchial thermoplasty (BT) is an endoscopic therapy employed for the treatment of refractory asthma. However, no predictive factors are available that determine the effectiveness of BT in treating asthma patients. The present study aimed to comprehensively analyze RNA samples from the airway bronchial tissues of 8 patients with severe asthma treated by BT, and to characterize each patient as a BT responder or non-responder. Total 24 RNA samples (three per patient prior to BT1 [baseline], prior to BT2 [after 1st time treatment], and prior to BT3 [after 2nd time treatment]) were obtained. There were 975 differentially expressed (DE) genes in the bronchial tissues of 8 patients between prior to BT1 (baseline) and prior to BT2 (after 1st time treatment), with significant differences (FDR-adjusted P<0.05). Subjects with an Asthma Quality of Life Questionnaire score change of >0.5 for a period of 12 months were considered BT responders. Non-responders exhibited a score change of <0.5 for 12 months. Transcriptome analysis at baseline identified 67 genes that were differentially expressed between responders and non-responders, including SLPI, MMP3, and MUC19 which were upregulated in responders.
2021-06-22 | GSE159091 | GEO
Project description:Purpose: The goal of this study is to investigate the alteration of gene expression pattern of alveolar macrophages by allergen challenge in human asthmatics. Method: By using subsegmental bronchial provocation with allergen (SBP-AG) protocol, we obtained BAL fluids, before and 48 hours after allergen challenge in the subjects enrolled in the protocol. Alveolar macrophages were purified from the BAL fluids and total RNA was isolated. Next-generation sequencing data were generated by using the Illumina system. Results: Using an optimized data analysis workflow, we mapped about 75 million sequence reads per sample to the human genome and identified 29,691 transcripts in the macrophage mRNAs. Among them, the change in the expression profiles of 37 transcripts were statistically significant. Conclusions: It has been well accepted that Th2 cytokine enriched environment transforms the phenotype of macrophages into alternatively activated form. However, the details of a genome-wide gene expression profiles of macrophages were not well investigated. Using RNA-seq technology, we provided comprehensive data of macrophage gene expression profiles in allergic lung inflammation. Our data could offer a framework to study biologic functions of alternatively activated macrophage in chronic inflammatory diseases. mRNA profiles of alveolar macrophages obtained from asthmatics, before and after allergen challenge.
2015-04-01 | E-GEOD-65039 | biostudies-arrayexpress
Project description: Not available
| S-EPMC8679176 | biostudies-literature