Expression of Neutrophil-related genes in patients with early sepsis-induced ARDS
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE66890 | GEO | 2015/04/01
SECONDARY ACCESSION(S): PRJNA278271
REPOSITORIES: GEO
Similar Datasets
Project description:Clinical study of critically ill patients with sepsis and sepsis-related ARDS with whole blood RNA collected within the first 24 hours of admission Goal of the study was to determine whether biologically relevant genes were identified to be differentially expressed genes in patients with sepsis alone and sepsis with ARDS Prospective observational study, case cohort design
2015-04-01 | E-GEOD-66890 | biostudies-arrayexpress
Project description:A microarray analysis involving whole blood samples isolated from critically ill patients in the medical intensive care unit at Brigham and Women's Hospital. Four groups of intubated subjects undergoing mechanical ventilation were recruited for the study: those with sepsis alone (Sepsis), those with sepsis + ARDS (se/ARDS), those with SIRS (SIRS), and those whithout sepsis, SIRS, or ARDS (untreated). Blood was obtained from patients on the day of admission (day 0) and 7 days later. RNA was isolated from the whole blood samples and microarrays were prepared to determine differential gene expression between the four groups. Total RNA obtained from whole blood samples of critically ill patients
2012-07-10 | E-GEOD-32707 | biostudies-arrayexpress
Project description:A microarray analysis involving whole blood samples isolated from critically ill patients in the medical intensive care unit at Brigham and Women's Hospital. Four groups of intubated subjects undergoing mechanical ventilation were recruited for the study: those with sepsis alone (Sepsis), those with sepsis + ARDS (se/ARDS), those with SIRS (SIRS), and those whithout sepsis, SIRS, or ARDS (untreated). Blood was obtained from patients on the day of admission (day 0) and 7 days later. RNA was isolated from the whole blood samples and microarrays were prepared to determine differential gene expression between the four groups.
2012-07-11 | GSE32707 | GEO
Project description:The Acute Respiratory Distress Syndrome (ARDS)/Acute Lung Injury (ALI) was described 30 years ago, yet the interaction between specific sets of genes involved in this syndrome remains incompletely understood. Experiment Overall Design: 13 patients with ALI + sepsis and 21 patients with sepsis alone were recruited from the Medical Intensive Care Unit of the University of Pittsburgh Medical Center between February 2005 and June 2007. Whole blood was obtained from each patient within 48 hours of admission, and RNA was extracted for gene expression profiling, and comparison analysis.
2008-04-09 | E-GEOD-10474 | biostudies-arrayexpress
Project description:The temporal evolution of sepsis was monitored by transcriptional profiling of five critically ill children with meningococcal sepsis and sepsis-induced multiple organ failure. Blood was sampled at 6 time points during the first 48 hours of their admission to pediatric intensive care, where the children received standard clinical treatment including organ support and antimicrobial therapy. Striking transcript instability was observed over the 48 hours, with increasing numbers of regulated genes over time. Most notably, proposed biomarkers for sepsis risk stratification also showed expression instability, with varied expression levels over 48 hours. This study demonstrates the extent of the complexity of temporal changes in gene expression that occur during the evolution of sepsis-induced multiple organ failure. Importantly, stratification tools that propose expression of biomarkers must take into account the temporal changes, over the use of single snapshots that may be less informative.
2013-04-03 | E-MEXP-3850 | biostudies-arrayexpress
Project description:Background: COVID-19 and sepsis represent formidable public health challenges, characterized by incompletely elucidated molecular mechanisms. Elucidating the interplay between COVID-19 and sepsis, particularly in geriatric patients suffering from sepsis-induced acute respiratory distress syndrome (ARDS), is of paramount importance for identifying potential therapeutic interventions to mitigate hospitalization and mortality risks.We employed bioinformatics and systems biology approaches to identify hub genes, shared pathways, molecular biomarkers, and candidate therapeutics for managing COVID-19, sepsis, and sepsis-induced ARDS. We corroborated these hub genes utilizing murine sepsis-ARDS models and blood samples derived from geriatric patients afflicted by sepsis-induced ARDS.Results: Our investigation revealed 189 differentially expressed genes (DEGs) shared among COVID-19 and sepsis datasets. We constructed a protein-protein interaction network, unearthing pivotal hub genes and modules. Notably, nine hub genes displayed significant alterations and correlations with critical inflammatory mediators of pulmonary injury in murine septic lungs. Simultaneously, 12 displayed significant changes and correlations with a neutrophil-recruiting chemokine in geriatric patients with sepsis-induced ARDS. Of these, six hub genes (CD247, CD2, CD40LG, KLRB1, LCN2, RETN) showed significant alterations across COVID-19, sepsis, and geriatric sepsis-induced ARDS. Our single-cell RNA sequencing analysis of hub genes across 3 diverse immune cell types furnished insights into disease pathogenesis. Functional analysis underscored the interconnection between sepsis/sepsis-ARDS and COVID-19, enabling us to pinpoint potential therapeutic targets, transcription factor-gene interactions, DEG-microRNA co-regulatory networks, and prospective drug and chemical compound interactions involving hub genes.Our investigation offers potential therapeutic targets/biomarkers, sheds light on the immune response in geriatric patients with sepsis-induced ARDS, emphasizes the association between sepsis/sepsis-ARDS and COVID-19, and proposes novel avenues for targeted therapies.
2023-09-01 | GSE242127 | GEO
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
Project description:Acute respiratory distress syndrome (ARDS) is a respiratory failure in critically ill patients, and the molecular mechanisms underlying its pathogenesis and severity are poorly understood. We evaluated mRNA and miRNA in patients with ARDS and elucidated the pathogenesis of ARDS, following mRNA and miRNA integration analysis. Thirty-four ARDS patients were compared with 15 healthy donors. 1233 mRNAs and 6 miRNAs were upregulated and 1580 mRNAs and 13 miRNAs were downregulated in ARDS patients compared healthy donors. In both mRNA and miRNA-targeted mRNA, the canonical pathway analysis showed that PD-1 and PD-L1 cancer immunotherapy pathway was most activated and Th2 pathway was most suppressed. miR-149-3p and several miRNAs were identified as upstream regulators. Integrated analysis of mRNAs and miRNAs showed that T cells were dysfunctional in ARDS patients.
2024-03-15 | GSE243067 | GEO
Project description:Acute respiratory distress syndrome (ARDS) is a respiratory failure in critically ill patients, and the molecular mechanisms underlying its pathogenesis and severity are poorly understood. We evaluated mRNA and miRNA in patients with ARDS and elucidated the pathogenesis of ARDS, following mRNA and miRNA integration analysis. Thirty-four ARDS patients were compared with 15 healthy donors. 1233 mRNAs and 6 miRNAs were upregulated and 1580 mRNAs and 13 miRNAs were downregulated in ARDS patients compared healthy donors. In both mRNA and miRNA-targeted mRNA, the canonical pathway analysis showed that PD-1 and PD-L1 cancer immunotherapy pathway was most activated and Th2 pathway was most suppressed. miR-149-3p and several miRNAs were identified as upstream regulators. Integrated analysis of mRNAs and miRNAs showed that T cells were dysfunctional in ARDS patients.
2024-03-15 | GSE243066 | GEO
Project description:In an endotoxaemic mouse model of sepsis, a tissue-based proteomics approach for biomarker discovery identified long pentraxin 3 (PTX3) as the lead candidate for inflamed myocardium. PTX3 accumulated as an octamer due to disulphide-bond formation in heart, kidney and lung ?common organ dysfunctions seen in patients with sepsis. Oligomeric moieties of PTX3 were also detectable in the circulation. The redox-state of PTX3 was quantified over the first 11 days in critically ill adult patients with sepsis. On admission day, there was no difference in the redox-state of PTX3 between survivors and non-survivors. From day 2 onwards, the conversion of octameric to monomeric PTX3 was consistently associated with a greater survival after 28 days of follow-up. For example, by day 2 post admission, octameric PTX3 was undetectable in survivors, but still constituted more than half of total PTX3 in non-survivors (P<0.001). Monomeric PTX3 was inversely associated with cardiac damage markers NT-proBNP, high sensitivity troponin I and T. In comparison to the conventional measurements of total PTX3 or NT-proBNP, the redox-sensitive oligomerization of PTX3 was more dynamic and a superior predictor of disease outcome.
2014-07-01 | PXD001020 | Pride