Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1081608 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28129624.fastq.gz | Fastqsanger.gz | |||
| SRR28129625.fastq.gz | Fastqsanger.gz | |||
| SRR28129626.fastq.gz | Fastqsanger.gz | |||
| SRR28129627.fastq.gz | Fastqsanger.gz | |||
| SRR28129628.fastq.gz | Fastqsanger.gz |
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Project description:Proteomics-based analysis of Peritoneal Dialysis Effluent is a relatively new approach to studying the changes associated with PD. Recent studies have shown altered proteomic profiles in various conditions of PD patients, including uremia, diabetes, peritonitis, abnormal peritoneal transport function and with different peritoneal dialysis modality. However, these studies extracted proteins in PDE by precipitation techniques resulting in high abundant diffusible proteins from blood circulation which interfered with the identification of low abundant, locally secreted, yet important, biomarkers. we hypothesize that EVs are secreted from peritoneal resident cells and contain known biomarkers for PDE-related membrane injury. As a proof of concept, here we identified and characterized EVs from PDE of healthy PD patients using transmission electron microscopy (TEM), dynamic light scattering (DLS), and nanoparticle tracking analysis (NTA). Furthermore, we did proteomics and bioinformatics analyses to determine the number and type of proteins measurable within EVs isolated from the PDE using two methods of vesicle isolation.
2018-08-14 | PXD006371 | Pride
Project description:In this open-label randomized controlled phase I/II trial, 20 stable peritoneal dialysis patients underwent two 4 h dwells with acidic glucose-based PDF, with and without 8 mM alanyl-glutamine (AlaGln) in a cross-over design. Unsupervised hierarchical clustering of transcriptomics data suggested specific effects of AlaGln in patients who had previously suffered from peritonitis.
2020-01-24 | GSE57070 | GEO
Project description:Bacterial infections and the concurrent inflammation have been associated with increased long-term cardiovascular (CV) risk. In patients receiving peritoneal dialysis (PD), bacterial peritonitis is a common occurrence, and each episode further increases late CV mortality risk. However, the underlying mechanism(s) remains to be elucidated before safe and efficient anti-inflammatory interventions can be developed. Damage-Associated Molecular Patterns (DAMPs) have been shown to contribute to the acute inflammatory response to infections, but a potential role for DAMPs in mediating long-term vascular inflammation and CV risk following infection resolution in PD, has not been investigated. We found that bacterial peritonitis in mice that resolved within 24h led to CV disease-promoting systemic and vascular immune-mediated inflammatory responses that were maintained up to 28 days. These included higher blood proportions of inflammatory leukocytes displaying increased adhesion molecule expression, higher plasma cytokines levels, and increased aortic inflammatory and atherosclerosis-associated gene expression. These effects were also observed in infected nephropathic mice and amplified in mice routinely exposed to PD fluids. A peritonitis episode resulted in elevated plasma levels of the DAMP Calprotectin, both in PD patients and mice, here the increase was maintained up to 28 days. In vitro, the ability of culture supernatants from infected cells to promote key inflammatory and atherosclerosis-associated cellular responses, such as monocyte chemotaxis, and foam cell formation, was Calprotectin-dependent. In vivo, Calprotectin blockade robustly inhibited the short and long-term peripheral and vascular consequences of peritonitis, thereby demonstrating that targeting of the DAMP Calprotectin is a promising therapeutic strategy to reduce the long-lasting vascular inflammatory aftermath of an infection, notably PD-associated peritonitis, ultimately lowering CV risk.
2023-11-22 | GSE246100 | GEO
Project description:Bacterial infections and the concurrent inflammation have been associated with increased long-term cardiovascular (CV) risk. In patients receiving peritoneal dialysis (PD), bacterial peritonitis is a common occurrence, and each episode further increases late CV mortality risk. However, the underlying mechanism(s) remains to be elucidated before safe and efficient anti-inflammatory interventions can be developed. Damage-Associated Molecular Patterns (DAMPs) have been shown to contribute to the acute inflammatory response to infections, but a potential role for DAMPs in mediating long-term vascular inflammation and CV risk following infection resolution in PD, has not been investigated. We found that bacterial peritonitis in mice that resolved within 24h led to CV disease-promoting systemic and vascular immune-mediated inflammatory responses that were maintained up to 28 days. These included higher blood proportions of inflammatory leukocytes displaying increased adhesion molecule expression, higher plasma cytokines levels, and increased aortic inflammatory and atherosclerosis-associated gene expression. These effects were also observed in infected nephropathic mice and amplified in mice routinely exposed to PD fluids. A peritonitis episode resulted in elevated plasma levels of the DAMP Calprotectin, both in PD patients and mice, here the increase was maintained up to 28 days. In vitro, the ability of culture supernatants from infected cells to promote key inflammatory and atherosclerosis-associated cellular responses, such as monocyte chemotaxis, and foam cell formation, was Calprotectin-dependent. In vivo, Calprotectin blockade robustly inhibited the short and long-term peripheral and vascular consequences of peritonitis, thereby demonstrating that targeting of the DAMP Calprotectin is a promising therapeutic strategy to reduce the long-lasting vascular inflammatory aftermath of an infection, notably PD-associated peritonitis, ultimately lowering CV risk.
2023-11-22 | GSE246101 | GEO
Project description:Cardiovasculopathy is the leading cause of death; patients with chronic kidney disease (CKD) are at particularly high risk. The pathophysiological role of accumulating reactive metabolites in CKD such as glucose degradation products (GDP) is uncertain. Large amounts of GDP are absorbed from conventional dialysis fluids in patients on chronic peritoneal dialysis (PD). Omental and parietal peritoneal tissues were obtained from 107 pediatric patients with CKD5 and 90 children on PD using dialysis fluids containing low and high concentrations of GDP, respectively. Fat surrounded omental arterioles, protected from local PD fluid exposure, were microdissected for transcriptome and proteome analyses.
2025-01-10 | E-MTAB-9646 | biostudies-arrayexpress
Project description:Peritoneal macrophages comprise two distinct subpopulations: large peritoneal macrophages (LPMs) and small peritoneal macrophages (SPMs), each with unique phenotypic and functional characteristics. This study investigates the role of retinoic acid (RA) in modulating the response of peritoneal macrophages to bacterial infections. Using a murine peritonitis model, we demonstrate that RA enhances the phagocytic capacity of macrophages, delays the decline in phagocytic function, and alters macrophage distribution in the peritoneal cavity. RA treatment induced notable transcriptional changes in both LPMs and SPMs.
2025-03-18 | GSE284043 | GEO
Project description:Transcriptome analysis of two population of peritoneal mononuclear phagocytes (CD14+ macrophages and CD1c+ dendritic cells) in peritoneal dialysis effluent from stable (infection-free) peritoneal dialysis patients.
2017-01-23 | E-MTAB-5439 | biostudies-arrayexpress
Project description:Peritoneal dialysis (PD) is a widely used kidney replacement therapy for patients with end-stage kidney disease. Nevertheless, long-term exposure to PD fluid can damage the peritoneal membrane, leading to ultrafiltration failure and, ultimately, discontinuation of PD. Investigation of the molecular mechanisms underlying this damage is essential for identifying new therapeutic targets to mitigate peritoneal deterioration in PD patients. To this end, we employed RNA sequencing in a preclinical model of peritoneal injury, induced by prolonged chlorhexidine (CHX) exposure, which revealed cytosolic DNA-sensing signaling as a novel pathway. Next, we demonstrated that key players in this pathway, such as the stimulator of interferon genes (STING) and its downstream signaling effectors (interferon regulatory factor 3, interferon-stimulated genes, and nuclear factor-κB signaling), were upregulated in experimental peritoneal damage. Moreover, increased STING expression was observed in human peritoneal biopsies from patients with PD. Subsequent studies in STING-deficient mice showed reduced proinflammatory gene expression and immune cell infiltration, together with inhibited nuclear factor-κB pathway activation at both early (10 days) and late (30 days) stages of CHX-induced peritoneal injury. STING deficiency also reduced peritoneal membrane thickening, fibrosis, and mesothelial-to-mesenchymal transition (MMT)-related changes in advanced CHX-induced damage. Furthermore, pharmacological inhibition of STING with C-176 attenuated CHX-induced peritoneal inflammation. Macrophages were identified as one of the STING-expressing cell types in the injured peritoneum. Hence, in vitro STING blockade in activated macrophages inhibited MMT in cultured mesothelial cells, suggesting that STING activation in this population may drive peritoneal fibrosis. Additionally, STING deficiency reduced peritoneal inflammation in S. epidermidis-induced peritonitis and decreased adhesion scores in a postsurgical intra-abdominal adhesion model. These findings identify STING as a pivotal mediator of peritoneal injury and support its potential as a novel therapeutic target to prevent PD-associated ultrafiltration failure. © 2025 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.
2024-11-25 | GSE282440 | GEO
Project description:Peritoneal mesothelial cells are harmed by peritoneal dialysis fluids (PDF) used in renal replacement therapy with peritoneal dialysis. The mechanisms of the cellular damage are not yet described in detail. Primary human peritoneal mesothelial cells derived from omentum of five donors were independently exposed to peritoneal dialysis fluids (extended recovery time). The extent of cell damage was assessed using lactate dehydrogenase (LDH) release in the cell culture supernatant and cells were lysed in order to extract mRNA and proteins. Transcriptional changes induced by PDF were analyzed using gene expression microarrays and changes of the proteome were analyzed using 2D-electrophoresis.
2019-12-31 | E-MTAB-7793 | biostudies-arrayexpress