Using RNA-Seq to investigate immune-metabolism features in immunocompromised patients with sepsis
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ABSTRACT:
PROVIDER: PRJNA756565 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15540614_1.fastq.gz | Fastqsanger.gz | |||
| SRR15540614_2.fastq.gz | Fastqsanger.gz | |||
| SRR15540615_1.fastq.gz | Fastqsanger.gz | |||
| SRR15540615_2.fastq.gz | Fastqsanger.gz | |||
| SRR15540616_1.fastq.gz | Fastqsanger.gz |
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Project description:Sepsis is life-threatening and leads to complex inflammation in immunocompromised subjects, including patients with cancer, those receiving immunosuppressants for autoimmune diseases and organ transplant recipients. Increasing evidence have shown that RNA-Sequencing (RNA-Seq) can be used to define subendotype in patients with sepsis; therefore, we aim to use RNA-Seq to identify transcriptomic features among immunocompromised patients with sepsis.
2021-08-23 | GSE182522 | GEO
Project description:Objective: Sepsis is life threatening and leads to complex inflammation in patients with immunocompromised conditions, such as cancer, and receiving immunosuppressants for autoimmune diseases and organ transplant recipients. Increasing evidence has shown that RNA-Sequencing (RNA-Seq) can be used to define subendotype in patients with sepsis; therefore, we aim to use RNA-Seq to identify transcriptomic features among immunocompromised patients with sepsis. Methods: We enrolled patients who were admitted to medical intensive care units (ICUs) for sepsis at a tertiary referral centre in central Taiwan. Whole blood on day-1 and day-8 was obtained for RNA-Seq. We used Gene Set Enrichment Analysis (GSEA) to identify the enriched pathway of day-8/day-1 differentially expressed genes and MiXCR to determine the diversity of T cell repertoire. Results: A total of 18 immunocompromised subjects with sepsis and 18 sequential organ failure assessment (SOFA) score-matched immunocompetent control subjects were enrolled. The ventilator-day, ICU-stay, and hospital-day were similar between the two groups, whereas the hospital mortality was higher in immunocompromised patients than those in immunocompetent patients (50.0 vs. 5.6%, p < 0.01). We found that the top day-8/day-1 upregulated genes in the immunocompetent group were mainly innate immunity and inflammation relevant genes, namely, PRSS33, HDC, ALOX15, FCER1A, and OLR1, whereas a blunted day-8/day-1 dynamic transcriptome was found among immunocompromised patients with septic. Functional pathway analyses of day-8/day-1 differentially expressed genes identified the upregulated functional biogenesis and T cell-associated pathways in immunocompetent patients recovered from sepsis, whereas merely downregulated metabolism-associated pathways were found in immunocompromised patients with septic. Moreover, we used MiXCR to identify a higher diversity of T cell receptor (TCR) in immunocompetent patients both on day-1 and on day-8 than those in immunocompromised patients. Conclusions: Using RNA-Seq, we found compromised T cell function, altered metabolic signalling, and decreased T cell diversity among immunocompromised patients with septic, and more mechanistic studies are warranted to elucidate the underlying mechanism.
| S-EPMC8718501 | biostudies-literature
Project description:Sepsis is a frequent complication in critically ill patients and highly heterogeneous that is associated with high morbidity and mortality rates, especially in the elderly population. Utilizing RNA-Sequencing (RNA-Seq) to analysis biological pathways is widely used in clinical and molecular genetics studies, but in elderly patients with sepsis are still lacking. Hence, we aim to investigate the mortality-relevant biological features and transcriptomic features in elderly patients who were admitted to intensive care unit (ICU) for sepsis.
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Project description:Polymorphonuclear cells show features of dysfunctional activation during fatal sepsis
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Project description:Sepsis and septic shock remain leading causes of morbidity and mortality for patients in Intensive care unit. In their early phase, immune cells produce various cytokines which lead to the prompt activation of the immune system. Polymorphonuclear leukocytes (PMNs) respond to different signals producing inflammatory factors and executing their antibacterial mechanisms, resulting in the engulfment and elimination of invading pathogens. However, long-term activation caused by various inflammatory signals produced during sepsis progression, can lead to the alteration of PMN signaling and subsequent defects in their functionality. Here we analyzed the PMNs samples from 34 patients in septic shock, we focused on PMNs gene expression and proteome changes caused by septic shock. We reveal that, compared to those of patients who survived, PMNs from patients who had a fulminant outcome were characterized by a dysfunctional hyper-activation, showing an altered metabolism, higher longevity and recent exit from cell cycle. We believe that this multi-omics approach, although limited, served to pinpoint the alterations in PMNs’ functionality, which may be reverted by targeted treatments.
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Project description:To investigate the differentially expressed genes in the plasma of pneumonia-induced sepsis patients compared to pneumonia patients without sepsis and healthy people, we performed gene expression profiling analysis using data obtained from RNA-seq.
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2013-08-31 | E-GEOD-23590 | biostudies-arrayexpress
Project description:Background: Sepsis involves aberrant immune responses to infection, but the exact nature of this immune dysfunction remains poorly defined. Bacterial endotoxins like lipopolysaccharide (LPS) are potent inducers of inflammation, which has been associated with the pathophysiology of sepsis, but repeated exposure can also induce a suppressive effect known as endotoxin tolerance or cellular reprogramming. It has been proposed that endotoxin tolerance might be associated with the immunosuppressive state that was primarily observed during late-stage sepsis. However, this relationship remains poorly characterised. Here we clarify the underlying mechanisms and timing of immune dysfunction in sepsis. Methods: We defined a gene expression signature characteristic of endotoxin tolerance. Gene-set test approaches were used to correlate this signature with early sepsis, both newly and retrospectively analysing microarrays from 593 patients in 11 cohorts. Then we recruited a unique cohort of possible sepsis patients at first clinical presentation in an independent blinded controlled observational study to determine whether this signature was associated with the development of confirmed sepsis and organ dysfunction. Findings: All sepsis patients presented an expression profile strongly associated with the endotoxin tolerance signature (p < 0.01; AUC 96.1%). Importantly, this signature further differentiated between suspected sepsis patients who did, or did not, go on to develop confirmed sepsis, and predicted the development of organ dysfunction. Interpretation: Our data support an updated model of sepsis pathogenesis in which endotoxin tolerance-mediated immune dysfunction (cellular reprogramming) is present throughout the clinical course of disease and related to disease severity. Thus endotoxin tolerance might offer new insights guiding the development of new therapies and diagnostics for early sepsis. For the RNA-Seq study reported here, 73 patients were recruited with deferred consent at the time of first examination in an emergency ward based on the opinion of physicians that there was a potential for the patient's condition to develop into sepsis. These were retrospectively divided into groups based on clinical features and compared to 11 non-urgent surgical controls.
2014-11-14 | E-GEOD-63311 | biostudies-arrayexpress
Project description:Impaired peripheral mononuclear cell metabolism in patients at risk of developing sepsis
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