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815 results for “pulmonary fibrosis”
Inhibition of epithelial cell YAP-TEAD/LOX signaling attenuates pulmonary fibrosis "
<table> <tbody> <tr> <td> <p>Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal disease characterized by excessive extracellular matrix (ECM) deposition. Current IPF therapies slow disease progression but do not stop or reverse it. The (myo)fibroblasts are thought to be the main cellular contributors to excessive ECM production in IPF. Here we report that fibrotic AT2 cells regulate production and crosslinking of ECM via the co-transcriptional activator YAP. YAP leads to increase expression of Lysyloxidase (LOX) and subsequent LOX mediated crosslinking by fibrotic AT2 cells. Pharmacological YAP inhibition reverses fibrotic AT2 cell reprogramming and LOX expression in experimental lung fibrosis <span>in vivo</span><span> and in human fibrotic </span><span>tissue ex vivo</span><span>. We thus identify YAP-TEAD/LOX inhibition in AT2 cells as a promising potential new therapy for IPF patients.<span> </span></span></p> <p><span><span>In</span></span></p> </td> </tr> </tbody> </table>
Data set for the publication entitled "Azithromycin alters spatial and temporal dynamics of airway microbiota in idiopathic pulmonary fibrosis"
<p>Set of files containing data used for microbiota analysis by 16S rRNA amplicon sequencing.</p> <p>The study cohort included patients with idiopathic pulmonary fibrosis from four centres in Switzerland, treated with azithromycin or placebo, sampled sequentially by oropharyngeal swab.</p> <p>This work is available in medRxiv and has been submitted</p>
Personalized in silico model for radiation-induced pulmonary fibrosis | (source code, simulation input+output data)
<p>This repository concerns the supplementary material data of the research article entitled "<em>Personalised in silico model for radiation-induced pulmonary fibrosis</em>" that is published in the Royal Society Interface journal (rsif.royalsocietypublishing.org). More specifically, the repository contains the source code of the radiation-induced pulmonary fibrosis simulator, the results produced from the medical image analysis of this study (CT scans and RT dosage maps) for each patient case, the input files necessary to run the simulator and the corresponding output produced respectively. Each patient ID corresponds to each case documented in the research article.</p>
Metabolic and lipidomic data of patients with idiopathic pulmonary fibrosis and healthy volunteers
<p>The metabolomic / lipidomic datasets used in the manuscript draft entiteld: </p> <p>"Changes in Serum Metabolomics in Idiopathic Pulmonary Fibrosis and effect of approved antifibrotic medication"</p> <p>by</p> <p>Benjamin Seeliger, Alfonso Carleo, Pedro David Wendel-Garcia, Jan Fuge, Ana Montes Worboys, Sven Schuchardt, Maria Molina-Molina and Antje Prasse</p> <p>Data is untransformed and missing data were imputated. All values are in µmol/L.</p>
Whole blood RNA-seq demonstrates an increased host immune response in individuals with cystic fibrosis who develop nontuberculous mycobacterial pulmonary disease
<p><strong>Background </strong></p> <p>Individuals with cystic fibrosis have an elevated lifetime risk of colonization, infection, and disease caused by nontuberculous mycobacteria. A prior study involving non-cystic fibrosis individuals reported a gene expression signature associated with susceptibility to nontuberculous mycobacteria pulmonary disease (NTM-PD). In this study, we determined whether people living with cystic fibrosis who progress to NTM-PD have a gene expression pattern similar to the one seen in the non-cystic fibrosis population. <strong> </strong></p> <p><strong>Methods</strong></p> <p>We evaluated whole blood transcriptomics using bulk RNA-seq in a cohort of cystic fibrosis patients with samples collected closest in timing to the first isolation of nontuberculous mycobacteria. The study population included patients who did (n = 12) and did not (n = 30) develop NTM-PD following the first mycobacterial growth. Progression to NTM-PD was defined by a consensus of two expert clinicians based on reviewing clinical, microbiological, and radiological information. Differential gene expression was determined by DESeq2.</p> <p><strong>Results</strong></p> <p>No differences in demographics or composition of white blood cell populations between groups were identified at baseline. Out of 213 genes associated with NTM-PD in the non-CF population, only two were significantly different in our cystic fibrosis NTM-PD cohort. Gene set enrichment analysis of the differential expression results showed that CF individuals who developed NTM-PD had higher expression levels of genes involved in the interferon (α and γ), tumor necrosis factor, and IL6-STAT3-JAK pathways. <strong> </strong></p> <p><strong>Conclusion</strong></p> <p>In contrast to the non-cystic fibrosis population, the gene expression signature of patients with cystic fibrosis who develop NTM-PD is characterized by increased innate immune responses.</p>
Dose-finding Study to Assess the Efficacy, Safety and Tolerability of Tobramycin Inhalation Powder in Patients With Non-Cystic Fibrosis Bronchiectasis and Pulmonary P. Aeruginosa Infection
ClinicalTrials.gov study NCT02712983. IPD Sharing: YES. Countries: 6. Publications: 2.
Enzyme-like nanoparticle engineered-mesenchymal stem cell secreting HGF promotes visualized therapy for idiopathic pulmonary fibrosis in vivo
Open the record for dataset details and reuse information.
Whole blood RNA-seq demonstrates an increased host immune response in individuals with cystic fibrosis who develop nontuberculous mycobacterial pulmonary disease
Open the record for dataset details and reuse information.
Emergence of inflammatory fibroblasts with aging in Hermansky-Pudlak syndrome associated pulmonary fibrosis
<p>The longitudinal cellular interactions that drive pulmonary fibrosis are not well understood. To investigate the disease underpinnings associated with fibrosis onset and progression, we generated a scRNAseq atlas of lungs from young and aged mouse models of multiple subtypes of Hermansky-Pudlak syndrome (HPS), a collection of rare autosomal recessive diseases associated with albinism, platelet dysfunction, and pulmonary fibrosis. We identified an age-dependent increase in SAA3<sup>+</sup> inflammatory lung fibroblasts in HPS mice, including in double-mutant HPS1-2 mice which develop spontaneous fibrosis. HPS1 fibroblasts showed increased expression of IL-1R1, whereas alveolar type II epithelial cells from HPS2 mice induced the inflammatory gene signature in co-cultured fibroblasts. scRNAseq of lung tissue from three HPS1 patients similarly showed the presence of inflammatory fibroblasts and increased <em>IL1R1</em> expression on fibroblasts. These data posit complex interactions between dysfunctional epithelial cells, inflammatory fibroblasts, and recruited immune cells, suggesting potential opportunities for mitigation of the fibrotic cascade. </p> <p>This record contains gzipped anndata h5ad (hdf5) files corresponding to the human scRNA-seq data analyzed during this study. One file (`adata_processed_data_generated_in_study_zenodo.h5ad`) contains only data derived from new samples processed in this study. Another file (`adata_processed_combined_zenodo.h5ad`) contains the aforementioned data from new samples, as well as data from previously published studies that are publicly available (Guo et. al., 2023, Tsukui et.al., 2022, Habermann et. al., 2020). Raw gene expression counts, as well as normalized counts, are provided as values in the `layers` attribute of the anndata object. Cell annotations and projection coordinates are similarly provided in the `obs` and `obsm` attributes of the object, respectively. The AnnData and Scanpy python libraries are required to load and re-process these data. </p>
Identification of early genes in the pathophysiology of fibrotic interstitial lung disease in a new model of pulmonary fibrosis
<p>Some interstitial lung diseases involve pulmonary fibrosis, which is a process that is characterized by the excessive and abnormal accumulation of extracellular matrix in the pulmonary interalveolar space. Although the current anti-fibrotic therapy aims at slowing down the progression of pulmonary fibrosis, it does not reverse it, and many of the drugs that were identified in basic-research studies failed in clinical phases, mainly because of the lack of a model that can recapitulate the pathophysiological mechanisms of human pulmonary fibrosis. We developed a novel experimental model of pulmonary fibrosis induced by a cocktail of molecules on an air/liquid interface culture of mouse embryonic lung explants. Histological analyses revealed a pattern of usual interstitial pneumonia, the worst-prognosis form of pulmonary fibrosis. We performed a transcriptomics analysis at the single-cell level after the induction of fibrosis and before any histological signs of fibrosis could be observed. The results revealed increased expression of several gene families that are involved in early inflammation, fibrosis and iron homeostasis, as well as potential new genetic targets.</p> <p>This Zenodo repository includes original datasets of single cell RNA sequencing, analysis R scripts, final dataset/markers, and HTML codes for the interactive 3D UMAP and VolcanoPlot.</p>
Hippo signaling impairs alveolar epithelial regeneration in pulmonary fibrosis
<p>Idiopathic pulmonary fibrosis (IPF) consists of fibrotic alveolar remodeling and progressive loss of pulmonary function. Genetic and experimental evidence indicates that chronic alveolar injury and failure to properly repair the respiratory epithelium are intrinsic to IPF pathogenesis. Loss of alveolar type 2 (AT2) stem cells or mutations that either impair their self-renewal and/or impair their differentiation into AT1 cells can serve as a trigger of pulmonary fibrosis. Recent reports indicate increased YAP activity in respiratory epithelial cells in IPF lungs. Individual IPF epithelial cells with aberrant Yap activation in bronchiolized regions frequently co-express AT1, AT2, conducting airway selective markers and even mesenchymal or EMT markers, demonstrating "indeterminate" states of differentiation and suggesting that aberrant Yap signaling might promote pulmonary fibrosis. Yet, Yap and Taz have recently also been shown to be important for AT1 cell maintenance and alveolar epithelial regeneration after <em>Streptococcus pneumoniae-</em>induced injury. To investigate how epithelial Yap/Taz might promote pulmonary fibrosis or drive alveolar epithelial regeneration, we inactivated the Hippo pathway in AT2 stem cells resulting in increased nuclear Yap/Taz and found that this promotes their alveolar regenerative capacity and reduces pulmonary fibrosis following bleomycin injury by pushing them along the AT1 cell lineage. Vice versa, inactivation of both Yap and Taz or Taz alone in AT2 stem cells impaired alveolar epithelial regeneration and resulted in increased pulmonary fibrosis upon bleomycin injury. Interestingly, inactivation of only Yap in AT2 stem cells promoted alveolar epithelial regeneration and reduced pulmonary fibrosis. Together, these data suggest that epithelial Yap promotes, and epithelial Taz reduces pulmonary fibrosis suggesting that targeting Yap- but not Taz-mediated transcription might help promote AT1 cell regeneration and treat pulmonary fibrosis.</p>
TKS5 mediates the formation of podosome rosettes in pulmonary fibroblasts and promotes fibrosis.
<p>Data and code for recreation of computationally-created figures of the paper: Barbayianni I., Kanellopoulou P. et al. <strong><em>SRC and TKS5-mediated podosome formation promotes Extracellular matrix invasion and pulmonary fibrosis</em></strong>. 2023</p> <p>Raw QuantSeq and re-analyzed single cell RNA-seq data can be found at GSE220982 and GSE122960, respectively.</p>
Combined PEX, Rituximab and Steroids in Acute Idiopathic Pulmonary Fibrosis Exacerbations
ClinicalTrials.gov study NCT01266317. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Fibroblast Specific Inhibition of LOXL2 and TGFbeta1 Signaling in Patients With Pulmonary Fibrosis.
ClinicalTrials.gov study NCT03928847. IPD Sharing: NO. Countries: 1. Publications: 2.
A Study of Lebrikizumab in Participants With Idiopathic Pulmonary Fibrosis (IPF)
ClinicalTrials.gov study NCT01872689. IPD Sharing: Not stated. Countries: 13. Publications: 1.
ARTEMIS-PH - Study of Ambrisentan in Subjects With Pulmonary Hypertension Associated With Idiopathic Pulmonary Fibrosis
ClinicalTrials.gov study NCT00879229. IPD Sharing: Not stated. Countries: 7. Publications: 1.
A Phase 1b Study of IV PRM151 in Patients With Idiopathic Pulmonary Fibrosis (IPF)
ClinicalTrials.gov study NCT01254409. IPD Sharing: Not stated. Countries: 2. Publications: 1.
Autoantibody Reduction for Acute Exacerbations of Idiopathic Pulmonary Fibrosis
ClinicalTrials.gov study NCT03286556. IPD Sharing: NO. Countries: 1. Publications: 10.
Safety and Efficacy of a Lysophosphatidic Acid Receptor Antagonist in Idiopathic Pulmonary Fibrosis
ClinicalTrials.gov study NCT01766817. IPD Sharing: Not stated. Countries: 6. Publications: 2.
Sildenafil Study to Treat Idiopathic Pulmonary Fibrosis
ClinicalTrials.gov study NCT00359736. IPD Sharing: Not stated. Countries: 1. Publications: 2.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.