Transcriptome analysis of microglia at day 3 and 20 following sepsis induction
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA817197 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18356503.fastq.gz | Fastqsanger.gz | |||
| SRR18356504.fastq.gz | Fastqsanger.gz | |||
| SRR18356505.fastq.gz | Fastqsanger.gz | |||
| SRR18356506.fastq.gz | Fastqsanger.gz | |||
| SRR18356507.fastq.gz | Fastqsanger.gz |
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Project description:Sepsis-associated encephalopathy is a common complication during systemic inflammation. Microglia are key player in this process. For a better understanding we compared isolated microglia from mice at day 3 and day 20 following induction of polymicrobial sepsis. We found a long-lasting inflammatory response of microglia following sepsis.
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Project description:Sepsis-associated encephalopathy is a common complication during systemic inflammation. Microglia are key player in this process. For a better understanding we compared hippocampal tissue following sepsis induction of microglia depleted and non-depleted mice. We show an overall reduction of inflammatory response in the hippocampus of microglia depleted animals.
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Project description:Lymphocytes are adversely affected during sepsis. Some CD4+ splenocytes undergo apoptosis while others become Th2 polarized. The molecular determinants of these phenotypic changes are not known. Here we compare the transcriptional response of septic CD4 splenocytes to CD4 splenocytes from sham-manipulated animals 6h after sepsis and identify an early transcriptional component to the septic CD4+ splenocyte phenotype. CD4+ splenocytes were isolated 6h after the surgical induction of sepsis for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain a homogeneous cell population in order to reduce any effects of cellular heterogeneity on expression profiles. To that end, immunomagnetic negative selection was used to enrich CD4+ splenocyte populations to ~91%. (n=5 biological replicates each CLP and sham)
2007-12-07 | E-GEOD-4479 | biostudies-arrayexpress
Project description:Ocular cytokine network plays pivotal role for initiation and progression of retinal degeneration, and microglia participate ocular inflammation. LPS activates MG5, mouse microglial cell line, and protein synthesis inhibitor CHX modulates cytokine expression pattern. To reveal comprehensive transition of molecular events, we performed proteome analysis using MG5 cells, and found that various mRNA modifying molecules are induced after LPS stimulation in addition to the inflammatory related molecules. The expression of mRNA modifying molecules are suppressed significantly by CHX, suggesting that transient induction of the molecules plays roles for determine the phenotype of inflammation in the microglia.
2025-02-26 | PXD050148 | JPOST Repository
Project description:Although in-hospital mortality rates for sepsis have decreased, survivors often experience lasting physical and cognitive deficits. Moreover, older adults are more vulnerable to long-term complications associated with sepsis. We employed a murine model to examine the influence of age and sex on the brain’s response and recovery following sepsis. Young (~4 months) and old (~20 months) mice (C57BL/6) of both sexes underwent cecal ligation and puncture (CLP) with restraint stress. The hippocampal transcriptome was examined in age and sex-matched controls at 1 and 4 days post-CLP. In general, immune and stress-related genes increased while neuronal, synaptic, and glial genes decreased one day after CLP-induced sepsis. However, specific age and sex differences were observed for the initial responsiveness to sepsis as well as the rate of recovery examined on day 4. Young females exhibited a muted transcriptional response relative to young males and old females. Old females exhibited a robust shift in gene transcription on day 1 and, while most genes recovered, genes linked to neurogenesis and myelination continued to be downregulated by day 4. In contrast, old males exhibited a more delayed or prolonged response to sepsis, such that neuronal and synaptic genes continued to decrease while immune response genes continued to increase on day 4. These results suggest that aging is associated with delayed recovery from sepsis, which is particularly evident in males.
2019-07-22 | GSE128925 | GEO
Project description:Sepsis, defined as a life-threatening organ dysfunction caused by a dysregulated host immune response to infection, is a common and dangerous clinical syndrome. Sepsis results in an excessive host inflammatory response that can induce immediate and persistent cognitive decline, and this is known to be worse in older individuals. Sex-specific differences in the outcome of infectious diseases and sepsis appear to favor females. These differences likely involve sex steroids, sex chromosomes, and possibly epigenetic mechanisms. We employed a murine model to examine the influence of age and sex on the brain's microRNA (miR) response following sepsis. Young (~ 4 months) and old (~ 20 months) adult mice (C57BL/6) of both sexes underwent cecal ligation and puncture (CLP) with daily restraint stress. Differential expression of hippocampal miR was examined in age- and sex-matched controls at 1 and 4 days post-CLP. A sexually dimorphic miR response was observed. Similar to previous work examining the transcription profile, young females exhibited a better recovery of the miR profile from day1 to day4, relative to young males and old females. For young males and all female groups, the initial response mainly involved a decrease in miR expression. In contrast, old males exhibited only upregulated miR on day1 and day4, with 22 miR upregulated across days. Examination of the relationship of these 22 upregulated miR with mRNA expression indicated downregulation of mRNA with time from induction of sepsis and was more pronounced for mRNA that were associated with multiple upregulated miR. The results emphasize age and sex differences in epigenetic mechanisms that likely contribute sexually dimorphic responses to sepsis.
2022-02-23 | GSE188874 | GEO
Project description:Sepsis is increasingly recognized as a major precipitant of long-term cognitive impairment, yet the cellular mechanisms underlying hippocampal vulnerability remain elusive. Using single-nucleus RNA sequencing of human hippocampal tissues from sepsis and control patients, we identied profound neurovascular alterations involving 21 distinct cell populations. Notably, astrocytes and microglia exhibited marked polarization: Astrocyte 2 showed simultaneous upregulation of neurotoxic A1 and neuroprotective A2 gene signatures in sepsis, whereas Astrocyte 1 displayed reduced A1 activity and a relatively quiescent pro le. In parallel, Microglia 2 demonstrated a prominent M1-like in ammatory signature, including elevated expression of HLA-DRA, IL1B, and TNF, while Microglia 1 downregulated both M1 and M2 markers, suggesting a hypo-responsive state. Intercellular communication analysis revealed intensi ed astrocyte–microglia interactions in the septic hippocampus, potentially amplifying in ammatory signaling loops. Concurrently, endothelial and mural cells exhibited transcriptional signatures of blood-brain barrier (BBB) disruption, oxidative stress, and compromised vascular homeostasis. Key molecular pathways associated with antigen presentation, cytokine signaling, and vascular permeability were selectively activated across neurovascular compartments. Together, our ndings uncover a coordinated glial and vascular response to systemic in ammation, driven in part by dysfunctional astrocyte–microglia crosstalk and pro-in ammatory polarization. These changes may underlie BBB breakdown and contribute to sustained neuroin ammation and cognitive decline in sepsis survivors. Targeting glial-vascular signaling axes and modulating astrocyte or microglial polarization states may offer promising avenues for therapeutic intervention in post-sepsis neurological sequelae.
2025-09-11 | GSE307512 | GEO
Project description:Sepsis is a syndromic response to infection and is frequently a final common pathway to death from many infectious diseases worldwide. The global burden of sepsis is difficult to ascertain, although a recent scientific publication estimated that there were 48.9 million cases and 11 million sepsis-related deaths worldwide, which accounted for almost 20% of all global deaths. Here we analyzed the whole blood transcriptome of 5 healthy controls and 5 patients with confirmed sepsis from the Department of Emergency, Division of Surgical critical care, Tongji Trauma Center, Tongji Hospital, Tongji Medical College. This research aims to understand the expression of immune cells in sepsis patients and to construct an immune cell landscape of sepsis.
2023-02-05 | GSE224095 | 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. Keywords: disease state analysis, gram-positive sepsis, gram-negative sepsis
2007-12-01 | GSE6535 | GEO
Project description:Purpose: We purified spinal cord microglia utilizing percoll gradients and magnetic beads, followed by transcriptome profiling (RNA-seq) to define microglia expression profiles against other neural, immune cell-types. We next observed how the microglial transcriptomes change during activation in the SOD1-G93A mouse model of motor neuron degeneration at 3 time points. We also compared these profiles with that induced by LPS injection. Results and conclusions: ALS microglia were found to differ substantially from those activated by LPS and from M1/M2 macrophages by comparison with published datasets. These ALS microglia showing substantial induction of a neurodegeneration-tailored phenotype, with induction of lysosomal, RNA splicing, and Alzheimer's disease pathway genes. Overall they express a mixture of neuroprotective and neurotoxic factors during activation in ALS mice, showing that neuro-immune activation in the spinal cord is a double-edged sword. We also detected the transcriptional nature of surface marker expression in microglia (CD11b, CD86, CD11c), and substantial T-cell microglia cross-talk using correlative microglia transcriptome/FACS analysis. 42 total RNA samples from purified spinal cord microglia were subjected to paired-end RNA-sequencing. Parallel flow cytometry data was collected from the same spinal cords.
2013-07-15 | E-GEOD-43366 | biostudies-arrayexpress