Altered gene expression in plasma of patients with pneumonia-induced sepsis compared to pneumonia without sepsis and healthy people
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE218494 | GEO | 2022/11/30
REPOSITORIES: GEO
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Project description:Altered gene expression in plasma of patients with pneumonia-induced sepsis compared to pneumonia without sepsis and healthy people
| PRJNA903936 | ENA
Project description:We here sought to firstly identify differentially abundant circulatory small non-coding RNA in critically ill patients with sepsis due to community-acquired pneumonia (CAP) patients as compared to healthy subjects, and secondly delineate those putatively targeted cellular pathways.
2021-08-18 | GSE137294 | GEO
Project description:We assayed leukocyte global gene expression for a prospective discovery cohort of 106 adult patients admitted to UK intensive care units with sepsis due to community acquired pneumonia or faecal peritonitis. We assigned all samples to sepsis response signature groups after performing unsupervised analysis of the transcriptomic data.
2017-05-01 | E-MTAB-5274 | biostudies-arrayexpress
Project description:We assayed leukocyte global gene expression for a prospective validation cohort of 221 adult patients admitted to UK intensive care units with sepsis due to community acquired pneumonia or faecal peritonitis. 10 samples from patients scheduled for elective cardiac surgery were also assayed as non-septic controls. We assigned all samples to sepsis response signature groups after performing unsupervised analysis of the transcriptomic data.
2017-05-01 | E-MTAB-5273 | biostudies-arrayexpress
Project description:Sepsis-induced acute lung injury (ALI) is prevalent in septic patients and has a high mortality rate. Considering ALI’s close link to sepsis, we used a Pseudomonas aeruginosa (PA) pneumonia-induced sepsis mouse model to investigate alveolar microenvironment alterations and lung injury post-sepsis. Peptidyl arginine deiminase (PADI) 2 and PADI4 are highly expressed in immune cells, and play substantial roles in the immune response to sepsis, but their specific functions remain unclear.We employed single-cell RNA sequencing (scRNA-seq) technology to map immune cell populations in bronchoalveolar lavage fluid (BALF) cells from Wild type (WT) and Padi2 and Padi4 double knock-out (DKO)mice in PA pneumonia-induced sepsis and sham conditions.
2024-11-30 | GSE274823 | GEO
Project description:Background: Community-acquired pneumonia (CAP) is defined as an acute lung infection involving the alveoli that occurs in a patient without recent health care exposure. A complication of CAP is severe sepsis, a syndrome of infection often accompanied by systemic inflammation and organ dysfunction. The aim of this study was to evaluate mRNA and miRNA in whole blood and to perform an integrative analysis to assess cellular signals that play a role in the pathogenesis of patients with CAP-associated sepsis. Methods: This was a prospective, observational, single-center study of patients transported to the Department of Traumatology and Acute Critical Medicine, Graduate School of Medicine, Osaka University. Patients with CAP-associated sepsis were analyzed. The diagnosis of pneumonia was made according to the clinical findings, including blood samples and chest computed tomography scan, and the diagnosis of sepsis followed the Sepsis-3 guidelines. Results: We included 14 critically ill patients with CAP-associated sepsis and 15 healthy control subjects (HCS). The median ages of the patient group and HCS were 78 and 55 years, and their body mass indexes were 22.8 and 21.7 kg/m2, respectively. All patients were treated at the critical care center, and 11 of the 14 patients received ventilatory management. All patients survived. These 14 patients met the diagnostic criteria of Sepsis-3 and were diagnosed as having CAP-associated sepsis. Of them, 6 patients met the diagnostic criteria for septic shock. RNA sequencing showed the number of genes with up:down (upregulated:downregulated) expression variation (false discovery rate [FDR] <0.05, |log2 fold change| >1.2) to be 1209:1461 for mRNA; 51:21 for microRNA; and 646:1274 for miRNA-targeted mRNA. Canonical pathway analysis using mRNA showed activation of the PD-1 and PD-L1 cancer immunotherapy signaling pathways and inhibition of the Th1 signaling pathway as well as that using miRNA-targeted mRNAs. Conclusions: Using integrated analysis of mRNA and miRNA, we elucidated for the first time, to our knowledge, that T-cell exhaustion occurred during the acute phase of CAP-associated sepsis and that miRNA regulated Th1 signaling and PD-1 and PD-L1 cancer immunotherapy signaling through the RNA interference action of mRNA.
2025-04-09 | GSE228541 | GEO
Project description:Background: Community-acquired pneumonia (CAP) is defined as an acute lung infection involving the alveoli that occurs in a patient without recent health care exposure. A complication of CAP is severe sepsis, a syndrome of infection often accompanied by systemic inflammation and organ dysfunction. The aim of this study was to evaluate mRNA and miRNA in whole blood and to perform an integrative analysis to assess cellular signals that play a role in the pathogenesis of patients with CAP-associated sepsis. Methods: This was a prospective, observational, single-center study of patients transported to the Department of Traumatology and Acute Critical Medicine, Graduate School of Medicine, Osaka University. Patients with CAP-associated sepsis were analyzed. The diagnosis of pneumonia was made according to the clinical findings, including blood samples and chest computed tomography scan, and the diagnosis of sepsis followed the Sepsis-3 guidelines. Results: We included 14 critically ill patients with CAP-associated sepsis and 15 healthy control subjects (HCS). The median ages of the patient group and HCS were 78 and 55 years, and their body mass indexes were 22.8 and 21.7 kg/m2, respectively. All patients were treated at the critical care center, and 11 of the 14 patients received ventilatory management. All patients survived. These 14 patients met the diagnostic criteria of Sepsis-3 and were diagnosed as having CAP-associated sepsis. Of them, 6 patients met the diagnostic criteria for septic shock. RNA sequencing showed the number of genes with up:down (upregulated:downregulated) expression variation (false discovery rate [FDR] <0.05, |log2 fold change| >1.2) to be 1209:1461 for mRNA; 51:21 for microRNA; and 646:1274 for miRNA-targeted mRNA. Canonical pathway analysis using mRNA showed activation of the PD-1 and PD-L1 cancer immunotherapy signaling pathways and inhibition of the Th1 signaling pathway as well as that using miRNA-targeted mRNAs. Conclusions: Using integrated analysis of mRNA and miRNA, we elucidated for the first time, to our knowledge, that T-cell exhaustion occurred during the acute phase of CAP-associated sepsis and that miRNA regulated Th1 signaling and PD-1 and PD-L1 cancer immunotherapy signaling through the RNA interference action of mRNA.
2025-04-09 | GSE228540 | GEO
Project description:To obtain novel biomarkers that serve as prompt indicators of sepsis, we aimed to screen out the differentially expressed miRNAs (DEMs) contribute to sepsis susceptibility and analyze the correlation of DEMs with inflammatory response. This case-control study included 40 sepsis patients and 40 physical examination donors as a control group. RNA-seq technology and bioinformatics analysis were used to screen out the DEMs between sepsis patients and normal people. The expression of these DEMs were subsequently verified by qRT-PCR. There were 305 DEMs (p<0. 05, |Fold change| ≥2) between sepsis and normal people were identified and top eighteen upregulated or downregulated miRNAs were picked out for QRT-PCR verification. Among them, 11 DEMs were high expression while 7 DEMs were low expression. Collectively, miRNA-3663-3p may be a potentially powerful diagnostic and predictive biomarker for sepsis.
2021-05-17 | GSE174507 | GEO
Project description:This study tested the hypothesis that recombinant granulocyte-macrophage colony-stimulating factor (rGM-CSF) enhances polymorphonuclear neutrophils (PMNs) via IL-1β to improve the prognosis of secondary infection in sepsis. The latter stage of sepsis is prone to induce immunosuppression, resulting in secondary fatal infections. rGM-CSF has become a way for sepsis-induced immunosuppression due to its immunomodulatory effect. However, the functional impact of GM-CSF on PMNs in sepsis remains obscure. This study aimed to study the role of rGM-CSF on the bactericidal ability of PMNs in septic mice, assessing its effect on the prognosis of secondary pneumonia, and explore the mechanism of rGM-CSF by intervening PMNs in patients with sepsis. The C57BL/6J sepsis mouse model was induced by cecal ligation and puncture (CLP). rmGM-CSF was used in vivo when mice developed immunosuppression, which was characterized by abnormal bactericidal function of PMNs in peripheral blood. rmGM-CSF improved the prognosis of secondary pneumonia and reversed the function of PMNs. PMNs isolated by Percoll from septic patients were treated by rhGM-CSF in vitro. The expression of CD11b, reactive oxygen species (ROS), phagocytosis and neutrophil extracellular traps (NETs) release in PMNs were enhanced by rhGM-CSF treatments. Whole-transcriptomic sequencing of mouse PMNs indicated that recombinant GM-CSF increased the expression of il1b gene in PMNs. Blocking and inhibiting IL-1β release effectively counteracted the enhancing effect of GM-CSF on the bactericidal function of PMNs. RmGM-CSF enhances the bactericidal function of PMNs in vivo and improves the prognosis of secondary pneumonia in septic mice, and recombinant GM-CSF increases IL-1β precursor reserves, which, if stimulated, can rapidly enhance the bactericidal capacity of PMNs.
2024-03-01 | GSE227162 | GEO
Project description:Sepsis is defined as a systemic inflammatory response secondary to a proven or suspected infection. Mechanisms governing this inflammatory response have been shown to be complex and dynamic, involving cross-talking among diverse signaling pathways. However, current knowledge on mechanisms underlying sepsis is far from providing a complete picture of the syndrome, justifying additional efforts that might add to this scenario. Microarray-based expression profiling is a powerful approach for the investigation of complex clinical conditions such as sepsis: the analysis of gene transcription at the genome level potentially avoids results derived from biased assumptions. In this study we investigate whole-genome gene expression profiles of mononuclear cells from survivor and non-survivor septic patients. Blood samples were collected at the time of sepsis diagnosis and seven days later, allowing us to evaluate the role of biological processes or genes possibly involved in patient recovery. Aiming to circumvent, at least partially, the heterogeneity of septic patients we included only patients admitted with sepsis caused by community-acquired pneumonia. Global gene expression profiling allowed us to characterize early sepsis, as compared to healthy individuals. Our results corroborate literature reports on inflammation response in the early stages of sepsis but highlight great heterogeneity in gene expression during sepsis progress. Additionally, global gene expression in the early stage was also able to distinguish sepsis from septic shock and correlated with patient outcome. Differences in oxidative stress seem to be associated with clinical outcome, since significant differences in the expression profile of related genes were observed between survivors and non-survivors at the time of patient enrollment (early sepsis). However, our results substantiate current knowledge supporting that sepsis syndrome development is indeed multifaceted. Although the initial infection of enrolled patients was pneumonia, seven days later gene expression profiles seemed to be characteristic of each patient, common gene expression changes distinguishing survivors from non-survivors. This result could be associated with the underlying health status of each one of them, with complications due to sepsis itself as well as with distinct timing for response to treatment. In this study we investigate whole-genome gene expression profiles of mononuclear cells from survivor (n=5) and non-survivor (n=5) septic patients, as well as from 3 healthy controls. Blood samples were collected at the time of sepsis diagnosis and seven days later, allowing us to evaluate the role of biological processes or genes possibly involved in patient recovery. Aiming to circumvent, at least partially, the heterogeneity of septic patients we included only patients admitted with sepsis caused by community-acquired pneumonia.
2014-06-20 | E-GEOD-48080 | biostudies-arrayexpress