Platelet transcriptome and high platelet turnover in sepsis
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ABSTRACT:
PROVIDER: PRJEB45262 | ENA |
REPOSITORIES: ENA
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Project description:Platelets and megakaryocytes are critical players in immune responses. Recent reports suggest infection and inflammation alter the megakaryocyte and platelet transcriptome to induce altered platelet reactivity. We examined if non-viral sepsis induces differential platelet gene expression and reactivity. Non-viral sepsis significantly upregulated IFITM3, an interferon responsive gene that restricts viral replication
2022-12-01 | GSE210797 | GEO
Project description:Relationships between platelet mitochondrial oxygen consumption rates (mOCR) and metabolites in platelets as measured by quantitative 1H-NMR metabolomics. Samples collected in ED at a single timepoint. WB and platelets isolated from the same blood samples. Comparison of mitochondrial function and metabolomics in patients with sepsis and non-sepsis ED patients
2019-12-13 | ST001294 | MetabolomicsWorkbench
Project description:Relationships between platelet mitochondrial oxygen consumption rates (mOCR) and metabolites in platelets as measured by quantitative 1H-NMR metabolomics in WB. Comparison of mitochondrial function and metabolomics in patients with sepsis and non-sepsis ED patients
2019-12-13 | ST001295 | MetabolomicsWorkbench
Project description:To explore the diverse platelet microRNA (miRNA) expression between high platelet reactivity (HPR) and low platelet reactivity (LPR) patients with acute coronary syndromes (ACS), we enrolled a cohort of ACS patients and performed miRNA expression profiling of platelets from four HPR and four LPR patients using human miRNA microarray system. VerifyNow P2Y12 assay was applied to indentify HPR and LPR. Venous blood was drawn from the patients and was centrifuged to prepare platelets. Among the candidate differentially expressed miRNAs, miR-15b expression was further confirmed to be lower in platelets of 22 HPR patients than 17 LPR by quantitative reverse-transcription polymerase chain reaction (RT-qPCR). We enrolled a consecutive cohort of 290 ACS patients and assessed the platelet reactivity using VerifyNow P2Y12 assay. In this study, HPR was defined as M-bM-^IM-%300 platelet reactivity unit (PRU) while LPR <170 PRU. miRNA microarray analysis was performed in platelets of four HPR and four LPR patients with ACS.
2014-07-17 | E-GEOD-59488 | biostudies-arrayexpress
Project description:To explore the diverse platelet microRNA (miRNA) expression between high platelet reactivity (HPR) and low platelet reactivity (LPR) patients with acute coronary syndromes (ACS), we enrolled a cohort of ACS patients and performed miRNA expression profiling of platelets from four HPR and four LPR patients using human miRNA microarray system. VerifyNow P2Y12 assay was applied to indentify HPR and LPR. Venous blood was drawn from the patients and was centrifuged to prepare platelets. Among the candidate differentially expressed miRNAs, miR-15b expression was further confirmed to be lower in platelets of 22 HPR patients than 17 LPR by quantitative reverse-transcription polymerase chain reaction (RT-qPCR).
2014-07-17 | GSE59488 | GEO
Project description:Platelets have a wide range of functions including critical roles in hemostasis, thrombosis, and immunity. We hypothesized that during acute inflammation, such as in life-threatening sepsis, there are fundamental changes in the sites of platelet production and phenotypes of resultant platelets. Here, we showed during sepsis that the spleen is a major site of megakaryopoiesis and platelet production. Sepsis provoked an adrenergic-dependent mobilization of megakaryocyte-erythrocyte progenitors (MEPs) from the bone marrow to the spleen where interleukin-3 (IL-3) induced their differentiation into megakaryocytes. In the spleen, immune-skewed megakaryocytes produced a CD40L-high platelet population with potent immunomodulatory functions. Transfusions of post-sepsis platelets enriched from splenic production enhanced immune responses and reduced overall mortality in sepsis-challenged animals. These findings identify a spleen-derived protective platelet population that may be broadly immunomodulatory in acute inflammatory states such as sepsis.
2022-02-14 | GSE196607 | GEO
Project description:Background: The role of viral infections as a mediator of systemic immune dysfunction leading to sepsis has received limited attention compared to the bacterial pathogens. The COVID-19 pandemic and the increased cases of sepsis in the absence of known bacterial pathogens have highlighted the clinical relevance of viruses as causative agents of sepsis. In this study, we investigated clinical, laboratory, proteomic, and metabolic characteristics to shed light on the molecular mechanisms underlying the pathological conditions of viral sepsis in COVID-19. Methods: We retrospectively analyzed data from 231 hospitalized patients with confirmed COVID-19 admitted to three hospitals in China. The presence of viral sepsis was diagnosed with SOFA score 2 in the absence of bacterial infection. Demographics, clinical, and laboratory parameters, as well as clinical outcomes, were obtained from electronic chart reviews. Plasma samples were obtained from a subset of these patients (23 patients in the Viral Non-Sepsis [VNS] group and 14 patients in the Viral Sepsis [VS] group) to analyze proteomic and metabolic profiles. Findings: The viral sepsis group exhibited severe disease, as indicated by elevated markers of both pulmonary (ARDS) and systemic disease (liver, kidney, and cardiac injury). Consistent with known immune paralysis observed in sepsis, subjects with viral sepsis were more susceptible to secondary infections by bacterial and fungal pathogens. Overall, viral sepsis led to an increased length of ICU stay, required invasive mechanical ventilation and a significant increase in mortality compared to the non-viral sepsis group. At the molecular levels, we identified unique metabolic and proteomic signatures that suggest a substantial contribution of the coagulation and platelet dysfunction pathways to systemic pathologies. Interpretation: Viral sepsis presents an underrecognized threat contributing to high mortality. Specific metabolic and proteomic changes demonstrated coagulation and platelet dysfunction as key pathological pathway in viral sepsis.
2024-03-03 | PXD050303 | iProX
Project description:Objective: It is unclear whether the host response of gram-positive sepsis differs from gram-negative sepsis at a transcriptome level. Using microarray technology, we compared the gene-expression profiles of gram-positive sepsis and gram-negative sepsis in critically ill patients. Design: A prospective cross-sectional study. Setting: A 20-bed general intensive care unit of a tertiary referral hospital. Patients: Seventy-two patients admitted to the intensive care unit. Interventions: Intravenous blood was collected for leukocyte separation and RNA extraction. Microarray experiements were then performed examing the expression level of 19,232 genes in each sample. Measurements and Main Results: There was no difference in the expression profile between gram-positive and gram-negative sepsis. The finding remained unchanged even when genes with lower expression level were included or after statistical stringency was lowered. There were, however, ninety-four genes differentially expressed between sepsis and control patients. These genes included those involved in immune regulation, inflammation and mitochondrial function. Hierarchical cluster analysis confirmed that the difference in gene expression profile existed between sepsis and control patients, but not between gram-positive and gram-negative patients. Conclusion: Gram-positive and gram-negative sepsis share a common host response at a transcriptome level. These findings support the hypothesis that the septic response is non-specific and is designed to provide a more general response that can be elicited by a wide range of different micro-organisms. Keywords: disease state analysis, gram-positive sepsis, gram-negative sepsis
2007-12-01 | GSE6535 | GEO
Project description: Not available
| S-EPMC8794123 | biostudies-literature
Project description:Objective: It is unclear whether the host response of gram-positive sepsis differs from gram-negative sepsis at a transcriptome level. Using microarray technology, we compared the gene-expression profiles of gram-positive sepsis and gram-negative sepsis in critically ill patients. Design: A prospective cross-sectional study. Setting: A 20-bed general intensive care unit of a tertiary referral hospital. Patients: Seventy-two patients admitted to the intensive care unit. Interventions: Intravenous blood was collected for leukocyte separation and RNA extraction. Microarray experiements were then performed examing the expression level of 19,232 genes in each sample. Measurements and Main Results: There was no difference in the expression profile between gram-positive and gram-negative sepsis. The finding remained unchanged even when genes with lower expression level were included or after statistical stringency was lowered. There were, however, ninety-four genes differentially expressed between sepsis and control patients. These genes included those involved in immune regulation, inflammation and mitochondrial function. Hierarchical cluster analysis confirmed that the difference in gene expression profile existed between sepsis and control patients, but not between gram-positive and gram-negative patients. Conclusion: Gram-positive and gram-negative sepsis share a common host response at a transcriptome level. These findings support the hypothesis that the septic response is non-specific and is designed to provide a more general response that can be elicited by a wide range of different micro-organisms. The study included seventy-two critically ill patients admitted to the intensive care unit (ICU) of Nepean Hospital, Sydney, Australia. Of these, fifty-five patients were diagnosed to have sepsis, as confirmed by microbiological culture. The remaining seventeen patients did not have sepsis and were therefore used as controls. The study was approved by the hospital ethics committee and informed consent was obtained from all patients or their relatives. Patient Samples. Whole blood was taken from each patient on admission to ICU. Neutrophils were separated from whole blood using density-gradient separation with Ficoll-PaqueP P(Amersham). Subsequent neutrophil RNA extraction was performed using guanidinium thiocyanate (Ambion). Microarray Experiment. The neutrophil RNA was converted to cDNA, fluorescently labeled and hybridized to its complimentary sequences on the microarray (Invitrogen). The fluorescent signals on each micrroarray were captured using the GenePix 4000B laser scanner (Axon Instruments). Expression level of each gene was represented by the intensity of its fluorescent signal. Data Extraction. All signal intensity values were processed using background-subtraction method. Prior to analysis, all values were log-transformed and normalized by fitting a print-tip group Lowess curve. Normalization minimizes bias due to dye chemistry, signal intensity or location of a gene on the array. It ensures the detection of genes that are truly differentially expressed, instead of those caused by experimental artifacts or variation in the hybridization process. After normalization, genes that had more than 50% of data missing were removed. We then selected genes that had at least 80% of the data showing two-fold changes from the geneâs median values. After filtering, 1617 genes were available for further analysis.
2010-05-25 | E-GEOD-6535 | biostudies-arrayexpress