Ontology highlight
ABSTRACT:
PROVIDER: PRJNA970939 | ENA |
REPOSITORIES: ENA
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Project description:Summary: Heart failure is frequently accompanied by pleural effusion, yet the biological impact of heart failure–associated pleural fluid on vascular endothelial function remains unclear. Here, we show that heart failure pleural fluid impairs endothelial barrier integrity and angiogenic capacity in human umbilical vein endothelial cells. Functional assays revealed increased permeability, reduced migration, and altered tube formation following treatment with patient-derived pleural fluid. Mechanistically, heart failure pleural fluid increased reactive oxygen species production and inflammatory signaling while downregulating tight junction protein ZO-1. Small RNA profiling identified miR 501 3p as a key mediator of these effects. Gain- and loss-of-function experiments demonstrated that miR 501 3p directly regulates ZO-1 expression and contributes to barrier disruption. These findings establish a microRNA-dependent mechanism linking heart failure pleural fluid to endothelial dysfunction and suggest a potential molecular pathway contributing to vascular complications in heart failure.
2026-03-12 | GSE319996 | GEO
Project description:Transcriptional profile comparison of the pleural and ascites fluids in hydropic fetuses affected with chylothorax. Two-condition experiment, pleural fluid vs. ascites fluid. Comparison of the transcriptional profile between sample collected before and after OK-432 treatment and between fetuses with and without a G404S mutation in the ITGA9 gene
2012-12-31 | E-GEOD-33872 | biostudies-arrayexpress
Project description:Pleural infection is a severe and complicated disease with increasing incidence worldwide and is characterised by substantial associated morbidity and mortality.1,2 Although it is accepted that the disease is heterogeneous, and there is a validated clinical prediction score (RAPID)3,4, the biological endotypes of pleural infection remain elusive and pleural fluid specific criteria to assess the intrapleural response are not available. A better understanding of pleural infection subtypes could lead to improved treatment strategies and clinical outcomes. All patients with pleural infection follow the same clinical journey which focusses on hospital admission, pleural fluid drainage and administration of antibiotics however, their recovery progress and clinical outcomes differ significantly.1,2 A subgroup of patients exhibits ineffective or failed intrapleural fibrinolysis leading to the development of fibrous septations which further complicates treatment. Consequently, approximately 30% of patients do not respond to treatment and require invasive treatments including surgical drainage. Tandem mass spectrometry is a high-throughput proteomics assay which is a reliable, unbiased, and hypothesis-free analytical method for investigating the underlying biology of disease using clinical specimens.5 The pleural fluid proteome faithfully reflects the intrapleural environment and could be utilised to identify disease key mediators, biomarkers, and treatment targets. For instance, pleural fluid pH, glucose and lactate dehydrogenase are used as clinical biochemistry markers for diagnosing patients with pleural infection.1 Our study (The Oxford Pleural Infection Endotyping Study, TORPIDS 2) applied mass spectrometry to pleural fluid specimens (n=80) from the PILOT trial.4 Our primary aims were to discover endotypes in pleural infection, characterise the intrapleural immune response and investigate the association between patient endotypes and high-precision bacterial patterns. We assessed the association between pleural infection endotypes and important clinical outcomes (1-year survival and need for surgery)
2026-02-23 | PXD054108 | Pride
Project description:Human fetal chylothorax: pleural fluid vs. ascites fluid
| PRJNA148361 | ENA
Project description:Analysis of the effect of human pleural fluid (HPF) or human serum albumin (HSA) on the transcriptome of Acinetobacter baumanii AB5075
2021-04-28 | GSE167117 | GEO
Project description:The mammalian immune system is constantly challenged by signals from both pathogenic and non-pathogenic microbes. Many of these non-pathogenic microbes have pathogenic potential if the immune system is compromised. The importance of type I interferons (IFNs) in orchestrating innate immune responses to pathogenic microbes has become clear in recent years. However, the control of opportunistic pathogens – and especially intracellular bacteria – by type I IFNs remains less appreciated. In this study, we use the opportunistic, Gram-negative bacterial pathogen Burkholderia cenocepacia (Bc) to show that type I IFNs are capable of limiting bacterial replication in macrophages, preventing illness in immunocompetent mice. Sustained type I IFN signaling through cytosolic receptors allows for increased expression of autophagy and linear ubiquitination mediators, which slows bacterial replication. Transcriptomic analyses and in vivo studies also show that LPS stimulation does not replicate the conditions of intracellular Gram-negative bacterial infection as it pertains to type I IFN stimulation or signaling. This study highlights the importance of type I IFNs in protection against opportunistic pathogens through innate immunity, without the need for damaging inflammatory responses.
2021-01-19 | GSE165020 | GEO
Project description:We profiled scRNA-seq of 284 samples collected from 196 individuals, including 22 patients with mild/moderate symptoms, 54 hospitalized patients with severe symptoms, and 95 recovered convalescent persons, as well as 25 healthy controls. The samples were obtained from various tissue types, including human peripheral blood mononuclear cells (249), bronchoalveolar lavage fluid (12) and pleural pleural effusion (1)/sputum (22).
2021-02-04 | GSE158055 | GEO
Project description:The opportunistic pathogen A. actinomycetemcomitans (Aa) expereinces fluctuating oxygen levels in its natural habitat, the gingival crevice of the human oral cavity. Since oxygen influences metabolic interactions between Aa and other oral microbes, we sought to characterize oxygen-dependent Aa gene expression.
2014-02-01 | E-MTAB-2213 | biostudies-arrayexpress
Project description:Streptococcus pneumoniae is the dominant cause of community-acquired pneumonia world-wide. Invasion of the pleural space is common and results in increased mortality. We set out to determine the bacterial and host factors that influence invasion of the pleural space. In a murine model of pneumococcal infection, we isolated neutrophil-dominated samples of bronchoalveolar and pleural fluid containing bacteria 48 hours after infection. Using dual RNA-seq, we characterised bacterial and host transcripts that were differentially regulated between these compartments and bacteria in broth and resting neutrophils respectively. Pleural and lung samples showed upregulation of genes involved in positive regulation of neutrophil extravasation but down-regulation of genes mediating bacterial killing. Compared to the lung samples, cells within the pleural space showed marked upregulation of many genes induced by type I interferons, cytokines implicated in preventing bacterial transmigration across epithelial barriers. Differences in the bacterial transcripts between the infected samples and bacteria grown in broth showed upregulation of genes in the bacteriocin locus, the pneumococcal surface adhesin PsaA, and the glycopeptide resistance gene, vanZ; the gene encoding the ClpP protease was downregulated in infection. 169 intergenic putative small bacterial RNAs were also identified, of which 43 (25.4%) had been previously described. 42 of the small RNAs were upregulated in pleura compared to broth, including many previously identified as important in virulence. Our results have identified key host and bacterial responses to invasion of the pleural space that can be potentially exploited to develop alternative antimicrobial strategies for prevention and treatment of pneumococcal pleural disease.
2019-07-11 | GSE134118 | GEO