Ontology highlight
ABSTRACT:
PROVIDER: PRJNA941079 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23702400_1.fastq.gz | Fastqsanger.gz | |||
| SRR23702400_2.fastq.gz | Fastqsanger.gz | |||
| SRR23702401_1.fastq.gz | Fastqsanger.gz | |||
| SRR23702401_2.fastq.gz | Fastqsanger.gz | |||
| SRR23702402_1.fastq.gz | Fastqsanger.gz |
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Project description:This repository contains human sample derived microbiome full-length 16S rRNA sequencing data for sputum samples in COPD patients. The project goal is to understand the association of the lung microbiome with accelerated lung function decline in COPD patients.
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Project description:<p>Progressive lung function decline is a hallmark of chronic obstructive pulmonary disease (COPD). Airway dysbiosis occurs in COPD, but whether it contributes to disease progression remains unknown. Here we showed, through a longitudinal analysis on two cohorts involving four UK centers, that baseline airway dysbiosis in COPD patients, characterized by enrichment of opportunistic pathogenic taxa, was associated with rapid forced expiratory volume in one second (FEV1) decline over two years. The dysbiosis was associated with exacerbation-related FEV1 fall and sudden FEV1 fall at stability, contributing to long-term FEV1 decline. The microbiota- FEV1-decline association was validated in a third cohort in China. Human multi-omics and murine studies showed that airway Staphylococcus aureus colonization promoted lung function decline through homocysteine, which elicited a neutrophil apoptosis-to-NETosis shift via AKT1-S100A8/A9 axis. S. aureus depletion via bacteriophages restored lung function in emphysema mice, providing a fresh approach to slow COPD progression by targeting airway microbiome.</p><p><br></p><p><strong>Linked studies:</strong></p><p><strong>UPLC-MS/MS assays</strong> of murine samples are reported in this study.</p><p><strong>UPLC-MS/MS assays</strong> of human samples are reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS5423' rel='noopener noreferrer' target='_blank'>MTBLS5423</a>.</p><p><strong>UPLC-MS/MS assays</strong> of original cohort human samples are reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS4017' rel='noopener noreferrer' target='_blank'>MTBLS4017</a>.</p>
2023-06-12 | MTBLS6894 | MetaboLights
Project description:<p>Progressive decline in lung function is a hallmark of chronic obstructive pulmonary disease (COPD). Although airway dysbiosis occurs in COPD, whether it contributes to disease progression remains unknown. Here, through a longitudinal analysis on 181 COPD individuals from two large cohorts involving four UK clinical centers, we showed that baseline airway dysbiosis, characterized by enrichment of opportunistic pathogenic taxa, was associated with rapid forced expiratory volume in one second (FEV1) decline over two years. Co-presence of Moraxella, Staphylococcus and Stenotrophomonas was associated with an accelerated FEV1 decline by 139.7 mL/year. The dysbiosis was associated with exacerbation-related FEV1 fall and sudden FEV1 fall at clinical stability, two critical events contributing to long-term FEV1 decline. The microbiota association with FEV1 decline was validated in a third, independent cohort in China. Human multi-omics, murine and cellular mechanistic studies showed that chronic airway colonization of Staphylococcus aureus promoted lung function decline through producing homocysteine, which elicited an apoptosis-to-NETosis shift in neutrophils toward persistent inflammation via AKT1-S100A8/A9 axis. Prophylactic and therapeutic depletion of S. aureus via bacteriophage restored lung function in emphysema mice. These results provide a fresh approach to slow COPD progression by targeting the airway microbiome.</p><p><br></p><p><strong>Linked studies:</strong></p><p><strong>UPLC-MS/MS assays</strong> of human samples are reported in this study.</p><p><strong>UPLC-MS/MS assays</strong> of murine samples are reported in<strong> </strong><a href='https://www.ebi.ac.uk/metabolights/MTBLS6894' rel='noopener noreferrer' target='_blank'><strong>MTBLS6894</strong></a>.</p><p><strong>UPLC-MS/MS assays</strong> of original cohort human samples are reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS4017' rel='noopener noreferrer' target='_blank'><strong>MTBLS4017</strong></a>.</p>
2023-06-12 | MTBLS5423 | MetaboLights
Project description:Chronic obstructive pulmonary disease (COPD) is characterized by a progressive decline in lung function, caused by exposure to exogenous particles, mainly cigarette smoke (CS). COPD pathogenesis is initiated and perpetuated by an abnormal CS-induced inflammatory response of the lungs, involving both innate and adaptive immunity. Specifically, B cells organized in iBALT structures, as well as macrophages, accumulate in the lungs and contribute to CS-induced emphysema, but the mechanisms thereof remain unclear. Here, we demonstrate that B cell-deficient mice are significantly protected against CS-induced emphysema. Chronic CS exposure led to increased lung compliance, total lung capacity, and mean linear chord length in WT, but not B cell-deficient mice, associated with an increased size and number of iBALT structures. The increased accumulation of macrophages around iBALT and in emphysematous alveolar areas in CS-exposed WT mice coincided with upregulated MMP12 expression. In vitro co-culture experiments using B cells and macrophages demonstrated that B cell-derived IL-10 drives macrophage activation and MMP12 upregulation. In summary, B cell function in iBALT formation in CS-induced emphysema provides a new innovative mechanism, which could be explored as a target for therapeutic intervention in COPD patients. Expression data of mice treated with cigarette smoke. Lung tissue was analysed at four and six months of age.
2014-12-04 | E-GEOD-52509 | biostudies-arrayexpress
Project description:Purpose: Build genesets using text mining and validate the geneset with data from public repository and a dataset generated in house using in vitro models and RNA-seq Methods: Mucus hypersecretion and mucociliary dysfucntion adverse outcome pathways (AOPs) genesets were build using the text mining method described by Rani et al., 2015. Validation was performed using RNA expression data from cigarette and e-cigarette aerosol treated cells, IL-13 treated airway cells, and COPD-lung biopsies. The cigarette and e-cigarette aerosol RNA-samples from airway cells were generated and sequenced in house. The other dataset were publically available. Results: Using unsupervised clustering, the mucus hypersecretion and mucociliary dysfunction genesets were able to discriminate the cigartte treated cells from the e-cigarettes and the air control. The e-cigarette and the air control clustered together. Clustering was also observed with IL-13 treated cells. IL-13 is an induced of mucus hypersecretion. Clustering was not observed when COPD RNA-seq samples were used. PCA analysis revealed some degree of grouping based on disease status, but this was also heavily confounded by other parameters. Conclusions: Our study described the first application of text mining to build genesets relevant to AOPs. In vitro validation confirmed the genesets could discriminates between treatment that induce mucus hypersecretion phenotypes, however this could not be confirmed with COPD biopsy samples. This could be due to a series of technical confouding factors and the heterogeneity of the COPD disease.
2020-04-30 | GSE142100 | GEO
Project description:Background: Chronic obstructive pulmonary disease (COPD) is a serious chronic disease of the airways that affects many people worldwide and have limited treatment options. While small animal models provide a platform for therapeutic investigations into COPD, their deficiencies continue to impede clinical translation. Alternatively, as a large animal model, sheep have a respiratory system anatomically and physiologically similar to that of humans, encouraging their use in airway disease research. The aim of this study was to better understand disease pathology in a large animal (sheep) experimental model of COPD. Methods: COPD was induced in sheep following lung exposure to porcine elastase (PE) and repeated weekly lung exposures to lipopolysaccharide (LPS) over a period of 8 weeks. Bronchoalveolar fluid and blood samples were collected for immune analyses. Lung function was assessed and lung tissues were collected for histopathology and RNA sequencing. Results: Lung neutrophil levels were elevated in response to repeated airway exposure to PE/LPS, accompanied by a significant decline in ventilation over time. Histological evidence of COPD-like disease changes included chronic inflammation with increased airway and tissue inflammation scores, together with significantly larger airway wall area measures, increased connective tissue deposition and dysregulated gene expression. Conclusions: These studies demonstrate sustained chronic airway inflammation and pathophysiological lung changes in a sheep model of COPD, providing many similarities to that seen in COPD patients. This work opens a pathway for future translational studies using this unique large animal model of COPD, which will serve to bridge the gap between smaller animal models and humans.
2023-12-31 | GSE242416 | GEO
Project description:<p> <p>The 'Genome-Wide Associations Environmental Interactions in the Lung Health Study' at Johns Hopkins University aims to test for association between lung function decline as a primary outcome associated with chronic obstructive pulmonary disease (COPD) using banked DNA and phenotype data on 4,287 European Americans from the longitudinal, multicenter Lung Health Study (LHS). The broad goals of the LungGO/ESP-GO falls into two general categories: (i) discovery of all variants (i.e., common and rare) in all protein-coding regions of the human genome (i.e., the exome) conferring risk to complex pulmonary diseases including COPD, in a subset of the LHS cohort. The Johns Hopkins University LHS cohort offers a unique opportunity to elucidate genetic variants that cause COPD.</p> <p>The Lung Health Study I was a randomized multicenter clinical trial with 5887 participants carried out from October 1986 to April 1994, designed to test the effectiveness of smoking cessation and bronchodilator administration in smokers aged 35 to 60 with mild lung function impairment. Participants were randomly assigned to one of three groups: <ul> <li>usual care, who received no intervention</li> <li>smoking intervention with the inhaled bronchodilator ipratroprium bromide</li> <li>smoking intervention with an inhaled placebo.</li> </ul> The effect of intervention was evaluated by the rate of decline of forced expiratory volume in one second (FEV1). </p> <p>For the GWAS, only the subset of European American LHS participants for whom lung function data from three time points or more are available. Thus, the GWAS represents 73% of the 5,887 volunteers who participated in the LHS study. Importantly, LHS subjects included had similar demographics (including age, gender and BMI) and rates of lung function decline (mean annual change in FEV1% predicted: -0.96 %/yr vs. -0.99 %/yr, p=0.57) compared with those not included in the GWAS, reflecting little selection bias for our primary outcome. They were, however, more likely to have quit smoking after 5 years.</p> <p>This study is part of the Gene Environment Association Studies initiative (GENEVA, <a href="http://www.genevastudy.org" target="_blank">http://www.genevastudy.org</a>) funded by the trans-NIH Genes, Environment, and Health Initiative (GEI). The overarching goal is to identify novel genetic factors that contribute to lung function through large-scale genome-wide association studies of smokers enrolled in a multicenter clinical trial. Genotyping was performed at the Johns Hopkins University Center for Inherited Disease Research (CIDR). Data cleaning and harmonization were done at the GEI-funded GENEVA Coordinating Center at the University of Washington.</p></p>
| phs000335 | dbGaP
Project description:Pathogenic interactions drive lung function decline.
| PRJEB75534 | ENA
Project description:Mucus accumulation is a key feature of respiratory diseases such as cystic fibrosis (CF) and chronic obstructive pulmonary disease (COPD). This is associated with goblet cell metaplasia and mucin overexpression, which can be induced by the increased activity of neutrophil elastase. The aim of the study was to characterization of mucus and epithelial cell proteomics in a porcine pancreatic elastase (PPE) mouse model of COPD/CF. The major proteins detected in mucus plugs obtained from PPE-treated mice included mucins Muc5ac and Muc5b, mucus-related proteins Clca1, Fcgbp, and Bpifb1. These proteins were upregulated in bronchoalveolar lavage (BAL) fluid and epithelial cells in mice exposed to elastase. Similar changes were found in BAL fluid of COPD patients.
2018-10-22 | PXD006770 | Pride
Project description:Chronic obstructive pulmonary disease (COPD) is associated with airway inflammation and microbiota dysbiosis. However, the function of lung microbiome alteration in early COPD remains unclear. This study is the first to characterize the lower respiratory tract microbiota in early COPD patients via bronchoalveolar lavage fluid (BALF) samples. By using full-length 16S sequencing, we found that the lung microbiome of early COPD patients had lower bacterial richness and significant compositional differences than did that of the healthy smoker controls. Streptococcus was the most robustly distinguished genus in early COPD patients and was associated with decreased lung function and increased host local inflammation. Furthermore, a murine cigarette smoke model of early COPD revealed that Streptococcus mitis promotes the progression of early COPD. Single-cell transcriptomics revealed that Streptococcus mitis increased emphysematous destruction of the lung parenchyma in a mouse early COPD model by regulating the function of alveolar type II (AT2) cells and macrophages. Therefore, targeting the lower airway microbiota in combination with smoking cessation may be a potential therapeutic approach for early COPD.
2025-03-02 | GSE290402 | GEO