Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1079996 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Our findings have clinical implications. Identification of sputum exosomal miRNA helps explore the important biological pathways underlying the pathogenesis of bronchiectasis, thus unraveling candidate targets for future interventions of PA colonization. Apart from canonical inflammatory pathways, we have unraveled the modulation of longevity regulation pathway which opens a new avenue for exploring how PA colonization interacts with the airway epithelium. The significant correlation between sputum inflammatory biomarkers and miR-92b-5p and miR-223-3p provided further evidence on the unresolved inflammation in the PA-colonized microenvironment. However, causality cannot be inferred based on the current study design.
2022-01-01 | GSE138820 | GEO
Project description:Microbiome sequencing of induced sputum and nasopharyngeal swabs from patients with bronchiectasis
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Project description:The aim of this study is to characterise and compare the composition of the microbiota from sputum samples of cystic fibrosis sufferers from different centres. These data are part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/
2014-09-16 | E-ERAD-265 | biostudies-arrayexpress
Project description:Bacterial microbiome of sputum samples from patients with bronchiectasis recruited in stable state
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Project description:Bacterial microbiome of sputum samples from patients with bronchiectasis recruited in stable state
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Project description:Non-cystic fibrosis bronchiectasis is a severe respiratory disease characterized by progressive loss of lung function, resulting in high morbidity and even early mortality. Current treatments cannot repair progressive lung damage, which encouraged the exploration of stem and progenitor cell-based regenerative therapies. In current study, we found that the P63+ progenitor cells normally located in airway basal layer could appear in the alveolar spaces of bronchiectasis patients. We successfully cloned and expanded the progenitor cells from the airway brushing tissues of patients. Then we conducted a randomized, single-blind, controlled, phase 1/2 trial to evaluate the safety and efficacy of autologous P63+ progenitor cells transplantation in bronchiectasis patients.
2024-10-15 | GSE261102 | GEO
Project description:Cystic fibrosis (CF) is an inherited, multi-system disease caused by dysfunction of the cystic fibrosis transmembrane conductance regulator (CFTR) protein, a ubiquitous ion channel important for epithelial hydration. A direct consequence of this dysfunction is impaired mucociliary clearance, chronic airway infection and a persistent neutrophilic inflammatory response that results in progressive loss of lung function, development of respiratory failure and premature death. Partial restoration of CFTR function is now possible for most CF patients through mutation specific CFTR modulators. Ivacaftor monotherapy produces significant clinical improvement in CF patients with the G511D mutation. Dual therapy, combining ivacaftor with lumacaftor or tezacaftor, results in modest clinical improvements in patients homozygous for F508del. More recently, triple therapy with elexacaftor/tezacaftor/ivacaftor (ETI) has led to dramatic improvements in lung function and quality of life in patients homozygous and heterozygous for F508del. Sputum proteomics is a powerful research technique capable of identifying important airway disease mechanisms by interrogating the proteome, an entire set of proteins within biological samples. It has confirmed the central role of neutrophilic immune dysregulation in CF and non-CF bronchiectasis, particularly involving the release of antimicrobial proteins and neutrophil-extracellular traps (NETs), and through impaired anti-inflammatory mechanisms. These processes produce distinct molecular signatures within the sputum proteome that become increasingly abnormal with chronic airway infection and progressive lung disease severity. In CF patients, airway and systemic inflammatory cytokines potentially related to these signatures reduce with the various forms of CFTR modulation. To date, no studies of ETI therapy in CF lung disease have assessed large-scale change in protein expression using untargeted proteomics. We hypothesised that ETI therapy would shift the sputum proteome toward health, potentially normalising airway biology in people with CF. The objectives of this study were to investigate changes in the CF sputum proteome with the introduction of ETI, correlate these with changes in clinical markers of disease severity, and make comparisons with the sputum proteome in healthy controls and in repeat samples from CF patients not suitable for ETI therapy. We also explored which molecular pathways associated with CF lung disease did not change with ETI.
2023-11-14 | PXD041950 | Pride