EPIMETRIC (EPIgenetic MEthylation-based Algorithm for Respiratory Illness Classification - COPD)
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE289742 | GEO | 2026/04/07
REPOSITORIES: GEO
Similar Datasets
Project description:Chronic obstructive pulmonary disease (COPD) is a highly prevalent disease leading to irreversible airflow limitation and is characterized by chronic pulmonary inflammation，obstructive bronchiolitis and emphysema. Etiologically, COPD is mediated by toxic gases and particles, e.g. cigarette smoke, while the pathogenesis of the disease is largely unknown. Several lines of evidence indicate a link between COPD and autoimmunity but comprehensive studies are lacking. By using a protein microarray assaying more than 19,000 human proteins we determined in this study the autoantibody profiles of COPD and non-COPD smokers.
2019-06-21 | GSE133096 | GEO
Project description:Activated eosinophils is a major cell type to be mainly involved in allergic diseases. Recent studies also indicated that eosinophils play an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD), especially asthma-COPD overlap and/or eosinophil COPD. The aim of this study is to clarify cellular characters of human eosinophils in patients with asthma-COPD overlap and/or eosinophil COPD.
2024-06-20 | PXD052550 | JPOST Repository
Project description:Rationale: DNA methylation is an epigenetic modification that is highly disrupted in response to cigarette smoke and involved in a wide spectrum of malignant and non-malignant diseases, but surprisingly not previously assessed in small airways of patients with chronic obstructive pulmonary disease (COPD). Small airways are the primary sites of airflow obstruction in COPD. We sought to determine whether DNA methylation patterns are disrupted in small airway epithelia of COPD patients, and evaluate whether changes in gene expression are associated with these disruptions. Methods: Genome-wide methylation and gene expression analysis were performed on small airway epithelial DNA and RNA obtained from the same patient during bronchoscopy, using Illumina's Infinium HM27 and Affymetrix's Genechip Human Gene 1.0 ST arrays. To control for known effects of cigarette smoking on DNA methylation, methylation and gene expression profiles were compared between former smokers (FS) with and without COPD matched for age, pack years and years of smoking cessation. Results: Our results indicate that aberrant DNA methylation is i) a genome-wide phenomenon in small airways of patients with COPD and ii) associated with altered expression of genes and pathways important to COPD, such as the Nrf2 oxidative response pathway. Conclusions: DNA methylation is likely an important mechanism contributing to modulation of genes important to COPD pathology. Since these methylation events may underlie disease-specific gene-expression changes, their characterization is a critical first step towards the development of epigenetic markers and an opportunity for developing novel epigenetic therapeutic interventions for COPD. Bisulphite converted DNA from small airway (airways less than <2 mm in diameter) from 38 former smokers: 15 subjects with COPD (post bronchodilator FEV1/FVC ratio <70% and FEV1 predicted M-bM-^IM-$ 80%) and 21 with normal lung function, were hybridized to the Illumina Infinium 27k Human Methylation Beadchip.
2014-02-28 | E-GEOD-55454 | biostudies-arrayexpress
Project description:Chronic inflammatory and immune dysregulation are critical drivers in the development and progression of chronic obstructive pulmonary disease (COPD). Posttranslational modifications, such as glycosylation of Immunoglobulin G (IgG), modulates systemic inflammatory homeostasis. This study aims to profile plasma IgG glycopeptides (IgGPs) in COPD patients to uncover new insights into its pathogenesis and to identify novel biomarkers. Plasma IgG N-glycopeptides from 90 COPD patients, 45 clinical defined early COPD (CECOPD) patients and 90 healthy individuals were analyzed using an integrated platform that combines Fe3O4@PDA@DETA nanospheres enrichment with high-resolution mass spectrometry measurement. Correlations between IgG N-glycoforms and clinical parameters were assessed to explore underlying mechanisms of COPD progression. Disease-specific IgGPs were identified in both ECOPD and COPD cohorts. Notably, IgG glyco-pattern, rather than IgG levels, changed with disease progression. Early COPD patients showed decreased bisection and increased site-specific afucosylated galactosylation and fucosylation of IgG, indicating an anti-inflammatory state. In contrast, COPD patients gave increased inflammation, characterized by reduced galactosylation and sialylation. Interestingly, a subset of healthy controls displayed IgGPs patterns similar to early COPD, possibly reflecting the impact of substantial smoking exposure and associated immune responses. These findings suggest that plasma IgG glycosylation could serve as a potential biomarker for early COPD diagnosis, providing valuable insights into immune system changes during disease progression.
2025-05-07 | PXD056374 | Pride
Project description:Rationale: DNA methylation is an epigenetic modification that is highly disrupted in response to cigarette smoke and involved in a wide spectrum of malignant and non-malignant diseases, but surprisingly not previously assessed in small airways of patients with chronic obstructive pulmonary disease (COPD). Small airways are the primary sites of airflow obstruction in COPD. We sought to determine whether DNA methylation patterns are disrupted in small airway epithelia of COPD patients, and evaluate whether changes in gene expression are associated with these disruptions. Methods: Genome-wide methylation and gene expression analysis were performed on small airway epithelial DNA and RNA obtained from the same patient during bronchoscopy, using Illumina's Infinium HM27 and Affymetrix's Genechip Human Gene 1.0 ST arrays. To control for known effects of cigarette smoking on DNA methylation, methylation and gene expression profiles were compared between former smokers (FS) with and without COPD matched for age, pack years and years of smoking cessation. Results: Our results indicate that aberrant DNA methylation is i) a genome-wide phenomenon in small airways of patients with COPD and ii) associated with altered expression of genes and pathways important to COPD, such as the Nrf2 oxidative response pathway. Conclusions: DNA methylation is likely an important mechanism contributing to modulation of genes important to COPD pathology. Since these methylation events may underlie disease-specific gene-expression changes, their characterization is a critical first step towards the development of epigenetic markers and an opportunity for developing novel epigenetic therapeutic interventions for COPD.
2014-02-28 | GSE55454 | GEO
Project description:Gene expression profiles in this submission were part of an integrative DNA methylation and gene expression integrative study. The goal of this study was to determine whether DNA methylation patterns were disrupted in small airway epithelia of patients with Chronic Obstructive Pulmonary Disease (COPD) compared to airways from subjects with normal lung function. No subject has cancer or asthma at time of collection. Corresponding DNA methylation profiles for these subjects can be found at GSE55454. We concluded that methylation alterations in COPD airways may underlie disease-specific gene-expression changes (such as the Nrf2 oxidative response pathway).
2014-03-28 | GSE56341 | GEO
Project description:Abstract<br>BACKGROUND: Gene expression profiling (GEP) in cells obtained from peripheral blood has demonstrated to be a very useful approach for biomarker discovery and for studying molecular pathogenesis of prevalent diseases. While there is limited literature availble on gene expression markers associated to Chronic Obstructive Pulmonary Disease (COPD), the transcriptomic picture associated to critical respiratory illness in this disease is not known to the present moment. <br>RESULTS: By using Agilent microarray chips, we have profiled gene expression signatures in whole blood of 28 COPD patients hospitalized with distinct degree of respiratory compromise.12 of them needed of admission to the ICU, while 16 were admitted to the Respiratory Medicine Service. GeneSpring GX 11.0 software was used for performing statistical comparison of transcript levels between ICU and non ICU patients. Ingenuity pathway analysis 8.5 (IPA) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) were employed to select, annotate and visualize genes by function and pathway (gene ontology). T-test evidenced 1501 genes differentially expressed between ICU and non ICU patients. IPA and KEGG analysis of the most representative biological functions revealed that ICU patients showed increased levels of neutrohil gene transcripts, being [cathepsin G (CTSG)], [elastase, neutrophil expressed (ELANE)], [proteinase 3 (PRTN3)], [myeloperoxidase (MPO)], [cathepsin D (CTSD)], [defensin, alpha 3, neutrophil-specific (DEFA3)], azurocidin 1 (AZU1)], [bactericidal/permeability-increasing protein (BPI)] the most representative ones. Proteins codified by these genes form part of the azurophilic granules of neutrophils and are involved in both antimicrobial defence and tissue damage. This ?neutrophil signature? was paralleled by necessity of advanced respiratory and vital support, and presence of bacterial infection.<br>CONCLUSION: study of transcriptomic signatures in blood suggests a central role of neutrophil proteases in COPD patients with critical respiratory illness. Measurement / modulation of the expression of these genes could represent an option for clinical monitoring and treatment of severe COPD exacerbations. <br><br>Keywords: COPD, critical, expression, gene, microarray, neutrophil, proteases.<br><br>
2013-03-12 | E-MEXP-3589 | biostudies-arrayexpress
Project description:Gene expression profiles in this submission were part of an integrative DNA methylation and gene expression integrative study. The goal of this study was to determine whether DNA methylation patterns were disrupted in small airway epithelia of patients with Chronic Obstructive Pulmonary Disease (COPD) compared to airways from subjects with normal lung function. No subject has cancer or asthma at time of collection. Corresponding DNA methylation profiles for these subjects can be found at GSE55454. We concluded that methylation alterations in COPD airways may underlie disease-specific gene-expression changes (such as the Nrf2 oxidative response pathway). RNA isolated from bronchial brushings was processed and hybridized to Affymetrix Human Gene 1.0 ST Arrays. DNA isolated from these same samples can be found at GSE55454
2014-03-28 | E-GEOD-56341 | biostudies-arrayexpress
Project description:Epigenetics changes have been shown to be affected by cigarette smoking. It is possible that cigarette smoke (CS)-mediated DNA methylation would affect several cellular and pathophysiological processes, acute exacerbations, and comorbidity in lungs of patients with chronic obstructive pulmonary disease (COPD). We sought to determine whether genome-wide lung DNA methylation profiles of smokers and patients with COPD were significantly different from non-smokers. We isolated DNA from lung tissues of patients including 8 lifelong non-smokers, 8 current smokers, and 8 patients with COPD, and subsequently analyzed the samples using the Illumina’s Infinium HumanMethylation450 BeadChip.
2017-06-12 | GSE92511 | GEO
Project description:Chronic obstructive pulmonary disease (COPD) Metagenome
| PRJNA647843 | ENA