Lung airway expression
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA833716 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This study seeks to characterize airway epithelial gene expression across small, medium and large airways in the normal human lung.
2024-04-07 | GSE201948 | GEO
Project description:Airway hyperresponsiveness is found to be a heritable trait and the parents of respiratory patients often have this trait. To understand if airway constriction affects the lung and contributes to lung disease, we investigated the lungs that often occur airway constriction and compared those lungs with healthy lung and the lung with inflammation.
2022-11-18 | GSE212406 | GEO
Project description:Supersulphides (inorganic and organic sulphides with sulphur catenation) manifest diverse physiological functions. These supersulphides are mainly generated from mitochondrial cysteinyl-tRNA synthetase (CARS2) that functions as a principal cysteine persulphide synthase (CPERS). Here we found powerful protective functions of supersulphides in viral airway infections (influenza and COVID-19) and chronic lung diseases, including chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF), and aged lungs. Enhanced supersulphide exhalation also occurred from human airways in COVID-19 as well as the hamster model of SARS-CoV-2 infection, as identified by breath supersulphur-omics that we developed herein. The lung damage related to oxidative stress and inflammation in mouse models of COPD, IPF, and ageing and the lethal effects that resulted were mitigated by endogenous supersulphides, supplied via CARS2/CPERS or exogenously by the supersulphide donor glutathione trisulphide. Our findings thus elucidated the airway protective role of supersulphides and their therapeutic potential in viral and chronic lung diseases.
2023-07-14 | PXD043607 | Pride
Project description:Cytologically normal airway epithelial samples were collected during bronchoscopy of current and former smokers. Subjects enrolled in this study were either under suspicion of having lung cancer, had dysplasia in their airway, or were a healthy current, former or never smoker. We supplemented existing GEO series (GSE4115 and GSE7895) with the samples in this study to explore PI3K pathway activity in the these cohorts. This study contains: 2 arrays from smokers with COPD (no lung cancer), 1 array from smoker without COPD (no lung cancer); 2 samples from patients with lung cancer, 2 samples from patients without lung cancer; 20 samples from 10 matched individuals with airway dysplasia before and after treatment with myo-inositol, 6 additional samples from individuals with airway dysplasia; 27 samples from mammary epithelial cells used in oncogenic pathway analysis that have either the PI3K pathway activated, the Np63 pathway activated, or are a GFP control.
2010-04-11 | E-GEOD-12815 | biostudies-arrayexpress
Project description:In this study, we assessed lower airway microbiome from a cohort of patients to determine whether specific microbiome taxa correlate with with specific metabolic activities. In a subset of 12 patients, transcriptomic expression were analyzed to compare host mucosa immune response We collected peripheral airway brushings from the 12 subjects whose lung microbiome were analyzed; Total RNA were obtained from the peripheral airway epithelium.
2016-03-29 | E-GEOD-73585 | biostudies-arrayexpress
Project description:Smoking-induced lung disease is one of the most prevalent forms of lung disease but also one of the more diverse. Based on the phenotypic diversity caused by the same environmental stress, we hypothesized that smoking may induce changes in lung cell expression of genes that, with specific variants, are causative of monogenic lung disease, i.e., not that smoking induces a phenocopy of a genetic disease, but smoking may subtly modify the expression of genes known to be associated with genetic disorders with distinct lung disease phenotypes. To assess this hypothesis, and based on the knowledge that most smoking-related disease phenotypes start in the small airway epithelium, we asked: are the genes associated with the monogenic lung disorders expressed in the small airway epithelium, and if so, does smoking alter the expression of these genes? To accomplish this, we examined small airway epithelium expression of 92 genes known to be associated with 17 monogenic lung disorders in 230 samples of small airway epithelium (SAE) obtained from healthy nonsmokers and healthy smokers without any clinical evidence of disease. Of the 86 monogenic disorder-related genes we found expressed in the SAE, strikingly, 37 were significantly differentially expressed in normal smokers compared to normal nonsmokers (p<0.05, Benjamini-Hochberg correction for multiple comparisons). The data demonstrates that the effect of smoking on the transcriptome of small airway epithelium includes significantly altered regulation of the genes responsible for known monogenic disorders.
2017-08-30 | GSE63127 | GEO
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:Introduction: Prenatal and postnatal cigarette smoke exposure enhances the risk of developing asthma. Despite this as well as other smoking related risks, 11% of women still smoke during pregnancy. We hypothesized that cigarette smoke exposure during prenatal development generates long lasting differential methylation altering transcriptional activity that correlates with disease. Methods: In a house dust mite (HDM) model of allergic airway disease, we measured airway hyperresponsiveness (AHR) and airway inflammation between mice exposed prenatally to cigarette smoke (CS) or filtered air (FA). DNA methylation and gene expression were then measured in lung tissue. Results: We demonstrate that HDM-treated CS mice develop a more severe allergic airway disease compared to HDM-treated FA mice including increased AHR and airway inflammation. While DNA methylation changes between the two HDM-treated groups failed to reach genome-wide significance, 99 DMRs had an uncorrected p-value < 0.001. 6 of these 99 DMRs were selected for validation, based on the immune function of adjacent genes, and only 2 of the 6 DMRs confirmed the bisulfite sequencing data. Additionally, genes near these 6 DMRs (Lif, Il27ra, Tle4, Ptk7, Nfatc2, and Runx3) are differentially expressed between HDM-treated CS mice and HDM-treated FA mice. Conclusions: Our findings confirm that prenatal exposure to cigarette smoke is sufficient to modify allergic airway disease, however, it is unlikely that specific methylation changes account for the exposure-response relationship. These findings highlight the important role in utero cigarette smoke exposure plays in the development of allergic airway disease. Lung DNA methylation profiles of mice exposed in utero to cigarette smoke (CS) then treated with house dust mite (HDM, n = 8) or saline (n = 6), or exposed in utero to filtered air (FA) then treated with HDM (n = 9) or saline (n = 6)
2015-11-19 | E-GEOD-71718 | biostudies-arrayexpress
Project description:To comprehensively study the heterogeneity within distal airway epithelium, we performed single cell transcriptomic analysis of the normal human donor lung samples. Our analysis reveals that secretory (club) and basal cells in the distal lung airway epithelial cells are highly heterogenous. Further interrogation of secretory cells identified a subpopulation with potential for alveolar differentiation in vitro, implicating distal lung airway secretory cells as new candidates in alveolar repair and regeneration.
2021-12-10 | GSE130076 | GEO
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