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LPS-stimulated endothelial cells using SILAC

ABSTRACT: Severe sepsis and septic shock, which occur with high incidence and are prevalent in the emergency department setting, are among the most common causes of death in hospitalized patients worldwide, and there has been a continuous increase in the incidence of sepsis of approximately 5–10% per year. Endothelial cells constitute an important metabolic organ in the physiological homeostasis of blood vessels and play a pivotal role in orchestrating the inflammatory response triggered by sepsis or endotoxemia. The secretome is defined as the subset of the proteome that contains all the proteins actively exported by a cell following a particular event.

INSTRUMENT(S): LTQ FT

ORGANISM(S): Homo Sapiens (ncbitaxon:9606)

SUBMITTER: Sangkyu Lee

PROVIDER: MSV000081707 | MassIVE | Fri Nov 10 12:18:00 GMT 2017

SECONDARY ACCESSION(S): PXD002220

REPOSITORIES: MassIVE

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Publications

In-depth proteomics approach of secretome to identify novel biomarker for sepsis in LPS-stimulated endothelial cells.

Kwon Oh Kwang OK Lee Wonhwa W Kim Sun Ju SJ Lee You-Mie YM Lee Ju Yeon JY Kim Jin Young JY Bae Jong-Sup JS Lee Sangkyu S

Electrophoresis 20150913 23

Sepsis and septic shock, which are conditions triggered by infection, occur with high incidence in emergency departments and are among the most common causes of death in hospitalized patients worldwide. Therefore, the identification of sepsis biomarkers for the rapid diagnosis is a major goal for researchers in the field of critical care. Endothelial cells play a pivotal role in orchestrating the inflammatory response triggered by sepsis. In this study, we used proteomics to investigate the secr ...[more]

PMID: 26257168

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LPS-stimulated endothelial cells using SILAC

Project description:Severe sepsis and septic shock, which occur with high incidence and are prevalent in the emergency department setting, are among the most common causes of death in hospitalized patients worldwide, and there has been a continuous increase in the incidence of sepsis of approximately 5–10% per year. Endothelial cells constitute an important metabolic organ in the physiological homeostasis of blood vessels and play a pivotal role in orchestrating the inflammatory response triggered by sepsis or endotoxemia. The secretome is defined as the subset of the proteome that contains all the proteins actively exported by a cell following a particular event.

2015-10-05 | PXD002220 | Pride

Comprehensive Landscape of SA-AKI Revealed by Integrated Proteomics and Metabolomics Analysis

Project description:Sepsis-associated acute kidney injury (SA-AKI) is a severe and life-threatening condi-tion with high morbidity and mortality among emergency patients, and it poses a sig-nificant risk of chronic renal failure. Clinical treatments for SA-AKI remain reactive and non-specific, lacking effective diagnostic biomarkers or treatment targets. In this study, we established an SA-AKI mouse model using LPS and performed proteomics and metabolomics analyses. A variety of bioinformatic analyses, including Gene Set En-richment Analysis (GSEA), Weighted Gene Co-expression Network Analysis (WGCNA), protein and protein interactions (PPI), and MetaboAnalyst analysis, were conducted to investigate the key molecules of SA-AKI. Proteomics and metabolomics analyses re-vealed that sepsis led to impaired renal mitochondrial function and metabolic disorders. Immune-related pathways were found to be activated in kidneys upon septic infection. The catabolic products of polyamines accumulated in septic kidneys. Overall, our study provides a more comprehensive understanding of SA-AKI and identifies potential pathways for this condition.

2023-10-24 | PXD044371 | Pride

Polyunsaturated dietary fats decrease mortality and bacterial load during septic S. aureus infection, and improve neutrophil function in mice

Project description:Severe infections and sepsis is an increasing clinical problem that cause prolonged morbidity and substantial mortality. At present, antibiotics are essentially the only pharmacological treatment for sepsis. The incidence of antibiotic resistance is increasing and it is therefore critical to find new therapies for sepsis. Staphylococcus aureus (S. aureus) is a major cause of septic mortality. Neutrophils play a major role in defense against bacterial infections. We have recently shown that a saturated high fat diet decreases survival in septic mice, but the mechanisms behind remain elusive. The aim of the present study was to investigate how the dietary fat composition affects survival and neutrophils function after experimental septic infection in mice. We found that, after S. aureus infection, mice fed polyunsaturated high fat diet (HFD/P) for 8 weeks had increased septic survival and decreased bacterial load compared with mice fed saturated HFD (HFD/S), and similar to that of mice given low fat diet (LFD). Furthermore, uninfected mice fed HFD/P had increased number of Ly6G+ neutrophils in bone marrow. In addition, mice fed HFD/P had a higher number Ly6G+ neutrophils recruited to the site of inflammation after peritoneal injection of thioglycollate. In conclusion, polyunsaturated dietary fat increased both survival and the efficiency of the bacterial clearance during septic S. aureus infection. Moreover, this diet enhanced the number and chemotaxis of neutrophils, a key component of the immune response to S. aureus infections. Mice (non-infected) fed saturated high fat diet, low fat diet, or polyunsaturated high fat diet

2014-11-24 | E-GEOD-58358 | biostudies-arrayexpress

Long non-coding RNA and mRNA expression profiles in rats with LPS-induced myocardial dysfunction

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Transcription profiling ofhuman pediatric systemic inflammatory response syndrome, sepsis, and septic shock spectrum

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Integrated lncRNAs and mRNAs sequencing reveals lncRNAs regulatory network associated with lung injury in LPS-induced septic shock rats

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2023-07-17 | GSE154653 | GEO

Beta 1 blockers improve survival and provide cardioprotection in septic mice

Project description:Septic cardiac dysfunction is a key feature of severe sepsis and septic shock, contributing to multiorgan dysfunction syndrome and death. It has been established that persistent beta adrenergic stimulation is detrimental in sepsis, and that specific beta 1 blockade mitigates excessive systemic inflammation and improves myocardial function. The aim of this study was to investigate the effects of specific beta 1 blocker esmolol on septic mouse myocardium by genomic and proteomic techniques. We also evaluated survival of septic mice and systemic inflammation under esmolol treatment. C57BL/6 mice were rendered septic by 2 models: cecal ligature and perforation (CLP) and intraperitoneal injection of lipopolysaccharides (LPS). Effects of esmolol on myocardium were assessed by microarray technique. Total RNA were isolated and purified from a 30mg sample of the heart of 6 groups of 8 animals, depending on the sepsis model and the treatment. The labeled cDNA from the treated animals were hybridized against the labeled cDNA from the untreated animals with 2 dye-swaps done for each sepsis model.

2015-08-03 | E-GEOD-31175 | biostudies-arrayexpress

Expression profiling across the pediatric systemic inflammatory response syndrome, sepsis, and septic shock spectrum

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Altered DNA methylation underlies monocyte dysregulation and immune exhaustion memory in sepsis [CUT&RUN]

Project description:Innate immune memory is the process by which pathogen exposure elicits cell-intrinsic states to alter the strength of future immune challenges. Such altered memory states drive monocyte dysregulation during sepsis, promoting pathogenic behavior characterized by pro-inflammatory, immunosuppressive gene expression and emergency hematopoiesis. Epigenetic changes, notably via histone modifications, have been shown to underlie innate immune memory, but the contribution of DNA methylation remains poorly understood. Using an ex vivo sepsis model, we discovered broad changes in DNA methylation throughout the genome of exhausted monocytes, including at several genes implicated in immune dysregulation during sepsis and Covid-19 infection (e.g. Plac8). Methylome reprogramming is driven in part by Wnt signaling inhibition in exhausted monocytes, and can be reversed with DNA methyltransferase inhibitors, Wnt agonists, or immune training molecules. These changes are recapitulated in septic mice following cecal slurry injection, supporting the involvement of DNA methylation in acute and long-term monocyte dysregulation during sepsis.

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