Sputum microbiome in COPD exacerbations
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ABSTRACT:
PROVIDER: PRJEB34697 | ENA |
REPOSITORIES: ENA
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Project description:Little is known about the lung microbiome dynamics and host-microbiome interactions in relation to chronic obstructive pulmonary disease (COPD) exacerbations and in patient subgroups based on smoking status and disease severity. Here we performed a 16S ribosomal RNA survey on sputum microbiome from 16 healthy and 43 COPD subjects. For COPD subjects, a longitudinal sampling was performed from stable state to exacerbations, at two and six weeks post-exacerbations and at six months from first stable visit. Host sputum transcriptome were characterized for a subset of COPD patient samples.
2021-03-21 | GSE112165 | GEO
Project description:Investigation of gene expression profiles among patients with COPD frequent exacerbations and to find gene targets as predictors of exacerbations COPD patient samples analysed by microarray, followed by PCR testing to identify gene predictors
2014-06-01 | E-GEOD-54837 | biostudies-arrayexpress
Project description:Investigation of gene expression profiles among patients with COPD frequent exacerbations and to find gene targets as predictors of exacerbations
2014-06-01 | GSE54837 | GEO
Project description:patients with acute COPD exacerbations Metagenome
| PRJNA631867 | ENA
Project description:We evaluated the applicability and usability of whole-genome methylomics of sputum samples in molecular profiling of chronic inflammatory lung diseases. Genomic DNA was purified from sputum samples of subjects with Asthma, COPD as well as healthy controls and analyzed on the Illumina Infinium HumanMethylation 450k platform.
2020-10-25 | GSE148000 | GEO
Project description:In addition to analyzing whole-genome methylation, we concomitantly evaluated sputum cell gene expression in the context of chronic inflammatory lung disease. Nucleic acids were purified from sputum samples of subjects with Asthma, COPD as well as healthy controls. Gene expression was analyzed on the Agilent Human GE 4x44k v2 platform.
2020-10-25 | GSE148004 | GEO
Project description:Background: Macrophages are important cells in pathogenesis of obstructive lung diseases including asthma and chronic obstructive pulmonary disease (COPD). The aim of the study was a multivariate, genetic, comparative analysis of macrophages from patients with asthma and COPD. Methods: Macrophages were isolated from induced sputum (IS) by magnetic bead separation. Transcriptomic measurements were carried out using Affymetrix Human Gene 2.1 ST ArrayStrip in 17 samples: 8 asthma (4 ICS naive , 4 ICS treated), 4 COPD and 5 control samples. The expression of the most significantly differentiating genes was evaluated by real time PCR in 34 samples (15 patients with asthma, 11 patients with COPD and 17 controls). Results: USP53 was the only gene differentially expressed (p adjusted clue =0.09) in the comparison between ICS naïve and ICS treated asthma. The PCR verification showed increased expression of BTF3, CDS2, DNAJC13, DDX5, GNAI2, SCGB1A1, SIRPB1, TRAF3IP, USP53, WDR49 in the asthma compared to COPD group. The changed gene expression profile of macrophages were characterized mostly by gene ontology terms linked with cell motility, cilium function, cell junction and adhesion organization. Conclusions: Gene expression profiling of sputum macrophages revealed distinct molecular capacity in asthma and COPD. The role of sputum macrophages in the pathophysiology of obstructive lung diseases is probably connected with biological processes associated with their motility, cilium dysfunction and cell junction organization.
2018-08-09 | GSE112260 | GEO
Project description:Lung infection by influenza A viruses is a common cause of disease exacerbations in patients with chronic obstructive pulmonary disease (COPD), however, this process is difficult to study in human patients. Here we used a microfluidic human lung airway-on-a-chip (Airway Chip) lined by primary human bronchial epithelium interfaced with primary human pulmonary microvascular endothelium to model this process in vitro. Airway Chips containing bronchial epithelial cells from COPD patients successfully replicated the increased sensitivity to the lung airway to infection by both influenza H1N1 and H3N2 viruses compared to chips lined by epithelium from healthy donors, including enhanced viral loads and increased production of inflammatory cytokines. Transcriptomics analysis of the healthy and COPD epithelium following infection with influenza H1N1 virus on-chip resulted in identification of several novel markers of COPD
2022-04-01 | GSE186908 | GEO
Project description:Chronic obstructive pulmonary disease (COPD) is one of the most prevalent lung diseases, and involves persistent airflow limitation and incorporates both emphysema and chronic bronchitis. Cigarette smoking has been identified as the main risk factor for disease development and progression. In a basic model of COPD, the disease is initiated when the physiologic response mechanisms to cigarette smoke exposure are overwhelmed; for example, because of long-term exposure effects or other aging-related changes. In this parallel-group case-controlled clinical study we asked to what extent the different transitions in a chronic-exposure-to-disease model are reflected in the proteome and cellular transcriptome of induced sputum samples from the lung. For this, we selected 60 age- and gender-matched individuals for each of four study groups: current healthy smokers, current-smoker COPD patients, former smokers, and never smokers (a total of 240 individuals). Induced sputum was collected, the cell-free supernatant was analyzed by quantitative proteomics (isobaric-tag based), and the cellular mRNA fraction was analyzed by microarray-based expression profiling. The sputum proteome of current smokers (healthy or COPD patients) clearly reflected the common physiological responses to smoke exposure, including alterations in mucin/trefoil proteins (e.g., MUC5AC and TFF1/3up-regulation), peptidase regulators (e.g., TIMP1 up-regulation), and a prominent xenobiotic/oxidative stress response (e.g., NQO1 and ALDH3A1 up-regulation). The latter response also was observed in the sputum transcriptome, which additionally demonstrated an immune-related polarization change (toward a M2 signature). The (long-term) former smoker group showed nearly complete reversal of the observable biological effects. Thirteen differentially abundant proteins between the COPD and healthy smoker groups were identified. These abundant proteins included previously reported COPD-associated proteins (e.g., TIMP1 (up-regulation) and APOA1 (down-regulation)) and novel proteins such as C6orf58 and BPIFB1 (LPLUNC1) (both up-regulated in the COPD group compared with the healthy smokers). In summary, our study demonstrates that sputum proteomics/transcriptomics can capture the complex and reversible physiological response to cigarette smoke exposure, which appears to be only slightly modulated in early-stage COPD patients. The study has been registered on ClinicalTrials.gov with identifier NCT01780298.
2015-08-28 | E-MTAB-3604 | biostudies-arrayexpress
Project description:In idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD), epithelial abnormalities are present including bronchiolization and alveolar cell death and dysfunction. As epithelial progenitor cells are directed by their microenvironment, we hypothesized that changes in the microenvironment disrupt normal epithelial growth and differentiation. We therefore mimicked the soluble factor microenvironment in IPF using an IPF cocktail (IPFc), composed of 9 factors which are increased in IPF lungs (CCL2, IL-1β, IL-4, IL-8, IL-13, IL-33, TGF-β, TNFα and TSLP) and in COPD exacerbations using an exacerbation cocktail (EC) composed of 4 factors that are increased during an exacerbation of COPD (TNFα, IL-1β, IL-6, IL-8). We asked whether the soluble factor milieu in IPF and COPD exacerbations affects epithelial growth and differentiation. Mouse lung organoids (primary EpCAM+ cells co-cultured with CCL206 fibroblasts) were used to study epithelial growth and differentiation. Organoids exposed to IPFc, EC or TGF-β (as a comparator) were resorted into EpCAM+ and CCL206 fractions, and subjected to RNA-sequencing.
2024-04-30 | GSE245259 | GEO