AEIPF Microbiome
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB18649 | ENA |
REPOSITORIES: ENA
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Project description:Viruses in acute exacerbations of idiopathic pulmonary fibrosis Keywords: viral detection BAL from patients with acute exacerbations of IPF and stable IPF were hybridized to a pan-viral cDNA microarray to evaluate the presence of virus during these episodes
2011-03-03 | E-GEOD-27578 | biostudies-arrayexpress
Project description:Viruses in acute exacerbations of idiopathic pulmonary fibrosis Keywords: viral detection
2011-03-03 | GSE27578 | GEO
Project description:Pulmonary fibrosis is a chronic progressive and often fatal disease. The pathogenesis is characterized by aberrant repair and remodeling of the lung parenchyma resulting in loss of physiological homeostasis, respiratory failure and death. The immune response in pulmonary fibrosis is dysregulated. The gut microbiome is a key regulator of immunity. The role of the gut microbiome in regulating the pulmonary immunity in lung fibrosis is unknown. Here, we have utilized a strategy of cage randomization to study how the horizontal transmission of gut microbiome influences the development of pulmonary fibrosis.
2022-07-29 | GSE209784 | GEO
Project description:Azithromycin (AZM) reduces pulmonary inflammation and exacerbations in chronic obstructive pulmonary disease patients with emphysema. The antimicrobial effects of AZM on the lung microbiome are not known and may contribute to its beneficial effects. Methods. Twenty smokers with emphysema were randomized to receive AZM 250 mg or placebo daily for 8 weeks. Bronchoalveolar lavage (BAL) was performed at baseline and after treatment. Measurements included: rDNA gene quantity and sequence. Results. Compared with placebo, AZM did not alter bacterial burden but reduced α-diversity, decreasing 11 low abundance taxa, none of which are classical pulmonary pathogens. Conclusions. AZM treatment the lung microbiome Randomized trial comparing azithromycin (AZM) treatment with placebo for eight weeks. Bronchoalveolar lavage (BAL) samples were obtained before and after treatment to explore the effects of AZM on microbiome, in the lower airways. 16S rRNA was quantified and sequenced (MiSeq) The amplicons from total 39 samples are barcoded and the barcode is provided in the metadata_complete.txt file.
2016-07-19 | E-GEOD-74396 | biostudies-arrayexpress
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:Azithromycin (AZM) reduces pulmonary inflammation and exacerbations in chronic obstructive pulmonary disease patients with emphysema. The antimicrobial effects of AZM on the lung microbiome are not known and may contribute to its beneficial effects. Methods. Twenty smokers with emphysema were randomized to receive AZM 250 mg or placebo daily for 8 weeks. Bronchoalveolar lavage (BAL) was performed at baseline and after treatment. Measurements included: rDNA gene quantity and sequence. Results. Compared with placebo, AZM did not alter bacterial burden but reduced α-diversity, decreasing 11 low abundance taxa, none of which are classical pulmonary pathogens. Conclusions. AZM treatment the lung microbiome
2016-07-19 | GSE74396 | GEO
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
Project description:LC-MS non-targeted metabolomics study of EBC samples from cystic fibrosis acute pulmonary exacerbations in adult and pediatric patients
2019-03-11 | ST001164 | MetabolomicsWorkbench
Project description:The clinical course of SARS-CoV-2 infection is highly variable with a subset of patients developing severe COVID-19 and acute respiratory distress syndrome (ARDS). COVID-19 induced lung injury and respiratory failure appears to be driven by dysregulated immune responses, yet the exact mechanisms remain unknown. Here, we analyzed monocytes isolated from healthy donors treated with SARS-CoV-2, influenza A (Panama strain) or TLR7/8 agonist R848. Notably, overnight exposure to SARS-CoV-2, but not influenza A virus, induced a profibrotic signature, characterized by high expression of known fibrogenic factors like TGFB1, SPP1 and LGMN, and showed highly significant similarity with profibrotic macrophage populations identified in idiopathic pulmonary fibrosis (IPF). In conclusion, SARS-CoV-2 triggers profibrotic macrophage responses, and ARDS-associated lung fibrosis.
2021-11-29 | PXD022709 | Pride