Identifying critical lncRNAs in PBMCs linked to sepsis-induced immunosuppression using microarray analysis
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ABSTRACT:
PROVIDER: PRJNA1207624 | ENA |
REPOSITORIES: ENA
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Project description:This study aims to identify key long non-coding RNAs (lncRNAs) and their associated pathways in peripheral blood mononuclear cells (PBMCs) from sepsis immunosuppression patients. Using weighted gene co-expression network analysis (WGCNA), we have constructed a co-expression network to elucidate the molecular mechanisms underlying sepsis-induced immunosuppression. The study utilizes Agilent Human ceRNA Microarray 2019 to profile lncRNA expression in PBMCs from three sepsis patients and three healthy controls.
2025-04-16 | GSE286082 | GEO
Project description:Background: Severe septic syndromes deeply impair innate and adaptive immunity. While neutrophils represent the first line of defense against infection, little is known about their phenotype and functions during sepsis-induced immunosuppression. The objective of this study was thus to perform for the first time a global evaluation of neutrophil alterations in immunosuppressed septic patients based on phenotypic, functional and transcriptomic studies. In addition, the potential association of these parameters and deleterious outcomes was assessed. Methods: Peripheral blood was collected from 9 septic shock patients at D3-4 and D6-8 presenting with features of sepsis-induced immunosuppression and compared to 8 healthy controls. Results: In order to get on overview of potential neutrophil alterations after sepsis, we performed transcriptomic analyses on purified neutrophils from 9 septic shock patients and 8 healthy volunteers. For each time point, comparisons were made between patients and controls. Venn diagrams indicated that 364 up-regulated genes and 328 down-regulated genes were common between the two analyses (Supplementary Tables 1 and 2). Interestingly, most of the differentially expressed genes are involved in cell maturation (CD177), apoptosis (STK4, Caspase 8), cell recruitment and chemotaxis (CD44, TPST, MMP9, CREB1), and antimicrobial properties (ARG1, STOM, ADAM9, CD63, YKL40) of neutrophils. Conclusions: The aim of the current study was to perform an extensive investigation of neutrophil alterations during sepsis-induced immunosuppression through phenotypic, functional and transcriptomic studies. Notably, transcriptomic study on purified neutrophils revealed differentially expressed genes between septic patients and healthy volunteers.
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Project description:We show a new immunosuppressive function for NKT cells, and the NKT cell-mTOR axis may be a therapeutic target to prevent post-sepsis immunosuppression
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Project description:Transcriptomes of human PBMCs and monocytes in sepsis patients
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Project description:Sepsis represents a complex disease with dysregulated inflammatory response and high mortality rate. Long noncoding RNAs (lncRNAs) have been reported to play regulatory roles in a variety of biological processes. However, studies evaluating the function of lncRNAs in pediatric sepsis are scarce, and current knowledge of the role of lncRNAs in pediatric sepsis is still limited. We explored the expression patterns of both lncRNAs and mRNAs between pediatric sepsis patients and healthy controls based on a comprehensive microarray analysis.
2020-02-14 | GSE145227 | GEO
Project description:Our experiments examined T-lymphocyte numbers and effector-functions in peritoneal contamination and infection (PCI) a mouse model of sepsis. One of our main questions was how T-lymphocytes reconstitute after sepsis-induced lymphopenia. We investigated the quantitative and qualitative recovery of T lymphocytes for 3.5 months after sepsis with or without IL-7 treatment. Sepsis is an immunological dysfunction against pathogens leading to inflammation with massive cytokine production. Simultaneously immunosuppression occurs e.g. lymphopenia, which is a hallmark of sepsis. The resulting immunosuppression is associated with secondary infections, which are often lethal. Moreover sepsis-survivors are burdened with increased morbidity and mortality for several years after the sepsis episode. The duration and clinical consequences of sepsis induced-immunosuppression are currently unknown. More than 50% of T-cells undergo apoptosis shortly after sepsis-induction. However, 8 days after sepsis onset, surviving mice present normal lymphocyte counts. Theoretically, T-cells could reconstitute in two different ways. Firstly, the diminished pool of T-cells is replenished by newly in thymus produced T-cells with new diverse T-cell-receptors (TCRs). Alternatively, remaining T-cells start to proliferate until reaching normal cell count. If this was the case all divided cells shared the same TCRs as primary cells. This could lead to a narrowed TCR diversity within a quantitative normalized T-cell pool and would be an explanation for the long-lasting immune incompetence. To address the question how T-cells recover from lymphopenia we applied next generation sequencing (NGS) to analyse TCR diversity in septic and healthy mice. One group of septic mice received Interleukin-7 (IL-7), an interleukin which regulates T-cell homeostasis and is a promising therapeutically approach for septic patients. 50000 sequences per mouse were analyzed and the three different groups (controls, sepsis, sepsis + IL-7 treatment) compared regarding their diversity. The sequenced raw data (fastq) are uploaded in this library.
2019-10-02 | E-MTAB-7483 | biostudies-arrayexpress
Project description:Sepsis is a debilitating disease with a worldwide prevalence. An increasing number of patients with sepsis, especially aged patients, suffer from chronic critical illness and develop persistent inflammation-immunosuppression and catabolism syndrome (PICS). Here, we profiled peripheral blood mononuclear cells in four patients with PICS, two patients with acute sepsis, and three healthy controls using single-cell RNA sequencing and systematic analyses. We found that gene expression patterns and developmental routes in distinct immune cell populations exhibited notable differences between patients with PICS, patients with acute sepsis, and healthy controls.
2025-01-23 | GSE217906 | GEO
Project description:The mechanisms underlying the increased mortality of secondary infections during the immunosuppressive phase of sepsis remain elusive. We established a mouse model of sepsis-induced immunosuppression followed by secondary infection. Compared to other organs, we observed a significant reduction in pro-inflammatory cytokines in the spleen, accompanied by a marked increase in IL-10 production, primarily by infiltrating neutrophils. Furthermore, we confirmed that these infiltrating neutrophils in the spleen during the immunosuppressive phase of sepsis undergo phenotypic change in the local microenvironment, exhibiting high expression of neutrophil biomarkers such as Siglec-F, Ly6G, and Siglec-E. These neutrophils subsequently produced IL-10 to suppress T lymphocytes. Depletion of neutrophils or specifically targeting Siglec-F leads to a notable improvement in the survival of mice with secondary infections. The identification of Siglec-F+ neutrophils as key regulators of immunosuppression following sepsis represents a novel finding with potential therapeutic implications.
2024-04-24 | GSE264139 | GEO