Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA241441 | ENA |
REPOSITORIES: ENA
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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:The apical junctional complex (AJC), composed of tight junctions and adherens junctions, is essential for maintaining epithelial barrier function. Since cigarette smoking and chronic obstructive pulmonary disease (COPD), the major smoking-induced disease, are both associated with increased lung epithelial permeability, we hypothesized that smoking alters the transcriptional program regulating AJC integrity in the small airway epithelium (SAE), the primary site of pathological changes in COPD. Transcriptome analysis revealed a global down-regulation of physiological AJC gene expression in the SAE of healthy smokers (n=53) compared to healthy nonsmokers (n=59), an observation associated with changes in molecular pathways regulating epithelial differentiation such as PTEN signaling and accompanied by induction of cancer-related AJC genes. Genome-wide co-expression analysis identified a smoking-sensitive AJC transcriptional network. The overall expression of AJC-associated genes was further decreased in COPD smokers (n=23). Exposure of human airway epithelial cells to cigarette smoke extract in vitro resulted in down-regulation of several AJC-related genes, accompanied by decreased transepithelial resistance. Thus, cigarette smoking alters the AJC gene expression architecture in the human airway epithelium, providing a molecular basis for the dysregulation of airway epithelial barrier function during the development of smoking-induced lung disease. The apical junctional complex (AJC), composed of tight junctions and adherens junctions, is essential for maintaining epithelial barrier function. Since cigarette smoking and chronic obstructive pulmonary disease (COPD), the major smoking-induced disease, are both associated with increased lung epithelial permeability, we hypothesized that smoking alters the transcriptional program regulating AJC integrity in the small airway epithelium (SAE), the primary site of pathological changes in COPD. In this study, microarray analysis of the SAE obtained from 53 healthy nonsmokers, 59 healthy smokers, and 23 smokers with COPD was performed to determine physiological AJC gene expression architecture in the SAE and its modification by cigarette smoking and during the development of COPD.
2011-06-27 | E-GEOD-20257 | biostudies-arrayexpress
Project description:Chronic obstructive pulmonary disease is a smoking-related disease that lacks effective therapies due partly to the poor understanding of disease pathogenesis. The aim of this study was to identify molecular pathways which could be responsible for the damaging consequences of smoking. To do this, we employed recently described bioinformatic methods to analyze differences in global gene expression, which we then related to the pathological changes induced by cigarette smoke (CS). Sprague-Dawley rats were exposed to whole-body CS for 1 day and for various periods up to 8 months. Experiment Overall Design: Timecourse with 12 timepoints with 8 replicates at each time point.
2008-06-15 | E-GEOD-7079 | biostudies-arrayexpress
Project description:Chronic obstructive pulmonary disease (COPD) Metagenome
| PRJNA647843 | ENA
Project description:Rationale: Chronic Obstructive Pulmonary Disease (COPD) is associated with a complex pulmonary and systemic immune response. Objective: To characterize and relate the lung tissue and circulating blood network immune response in COPD. Methods: Lung tissue and circulating blood samples were simultaneously obtained from COPD patients (current smokers n=28 and former smokers n=16) and controls (current smokers n=9 and non-smokers n=12) undergoing thoracic surgery. We used flow cytometry to assess the immune cell composition, Affymetrix arrays to determine whole lung mRNA expression, and Weighted Gene Co-expression Network Analysis (WGCNA) to characterize and compare the pulmonary and systemic immune responses in patients and controls. Results: In lung tissue of current smokers with COPD (vs. non-smokers and former smokers with COPD) we observed a significant increase in the proportion of intermediated phenotype macrophages (Mphage) expressing both M1 and M2 markers, whereas that of M1 Mphage (pro-inflammatory) and CD4+ and CD8+ T-lymphocytes were decreased. These changes were not mirrored in circulating blood but WGCNA identified three modules of co-expressed genes that related, respectively to: (1) the total proportion of lung Mphage (extracellular matrix and angiogenesis genes) ; (2) active smoking (T cell and apoptosis related genes); and, (3) severity of airflow limitation (cilium organization genes). Conclusions: In mild/moderate COPD, the main pulmonary immune cell alterations relate to current smoking, involve changes in the proportion of Mphage and T cells and are associated with changes in whole lung tissue transcriptome. These cellular pulmonary changes are not mirrored in the systemic circulation.
2018-07-01 | GSE103174 | GEO
Project description:Chronic obstructive pulmonary disease is a smoking-related disease that lacks effective therapies due partly to the poor understanding of disease pathogenesis. The aim of this study was to identify molecular pathways which could be responsible for the damaging consequences of smoking. To do this, we employed recently described bioinformatic methods to analyze differences in global gene expression, which we then related to the pathological changes induced by cigarette smoke (CS). Sprague-Dawley rats were exposed to whole-body CS for 1 day and for various periods up to 8 months. Keywords: Timecourse
2007-12-11 | GSE7079 | GEO
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:Expression analysis of stable chronic obstructive pulmonary disease and acute exacerbation of chronic obstructive pulmonary disease
| PRJNA258183 | ENA
Project description:Lymphotoxin β-receptor-signalling orchestrates lymphoid neogenesis and subsequent tertiary lymphoid structures (TLS) associated with severe chronic inflammatory diseases spanning multiple organ systems. How LTβR-signalling drives chronic tissue damage particularly in the lung, which mechanism(s) regulate this process, and whether LTβR-blockade might be of therapeutic value has remained unclear. Here we demonstrate increased lymphotoxin expression of LTbR-ligands on myeloid and adaptive and innate immune-cells, enhanced non-canonical NF-κB signalling and enrichment of LTβR-target gene expression in epithelial cells of lungs from patients and mice with smoking-associated chronic obstructive pulmonary disease (COPD). Accordingly, Therapeutic inhibition of LTβR-signalling in young and aged mice with COPD disrupted TLS, reverted lung tissue destruction, airway-fibrosis and systemic muscle wasting. Mechanistically, we identified that LTβR-signalling blockade leads to diminished cell-death, concomitantly reactivated endogenous Wnt/β-catenin-signalling in alveolar epithelial cells and reduced TGFβ-signalling in airways. These findings highlight LTβR as a viable therapeutic target against TLS induced tissue damage that translates into novel anti-inflammatory, regenerative strategies to treat COPD.
2020-07-10 | GSE125521 | GEO