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Single cell transcriptomics of human brain epileptic lesions identifies pro-inflammatory immune mechanisms based on interlacing cellular immune networks

ABSTRACT: Single cell transcriptomics of human brain epileptic lesions identifies pro-inflammatory immune mechanisms based on interlacing cellular immune networks

PROVIDER: PRJNA828149 | ENA |

REPOSITORIES: ENA

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Single cell transcriptomics of human brain epileptic lesions identifies pro-inflammatory immune mechanisms based on interlacing cellular immune networks

Project description:We analysed 85780 single cells from epileptic brain tissues using Cellular Indexing of Transcriptomes and Epitopes by Sequencing (CITE-seq) to dissect the architecture of the immuno-transcriptome of the diseased epileptic human brain. dissect the architecture of the immuno-transcriptome of the diseased epileptic human brain. Our approach uncovered in all patients, well organized pro-inflammatory microenvironment pivoting on activated, pro-inflammatory microglia in a closely-knit network where resident cells attract and manipulate in a pro-inflammatory fashion infiltrating innate and adaptive immune cells. These findings were corroborated by ligand-receptor interactome analysis, which demonstrated potential mechanisms of infiltration and by evidence of direct interactions between microglia and T cells likely contributing to pathogenesis.

2022-04-20 | GSE201048 | GEO

Rat MeDIP Array, naïve, epileptic, and adenosine treated

Project description:Epilepsy causes altered gene expression; transient adenosine treatment inhibits progression of epileptogenesis Hippocampus of epileptic rat is hypermethylated compared to naïve; adenosine treatment causes hypomethylation Metylation state in epileptic rats (9 weeks post kainic acid induced status epilepticus) was compared to naïve (untreated) rats and epileptic rats treated with adenosine for 5 days

2013-09-05 | E-GEOD-45932 | biostudies-arrayexpress

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Project description:Digital dermatitis is a painful foot disease compromising welfare in dairy cattle. The disease has a complex multibacterial aetiology, but little is known about its pathogenesis. In this study, gene expression in skin biopsies from five bovine digital dermatitis lesions and five healthy bovine feet was compared using RNA-Seq technology. Differential gene expression was determined after mapping transcripts to the Btau 4.0 genome. Pathway analysis identified gene networks involving differentially expressed transcripts. Bovine digital dermatitis lesions had increased expression of mRNA for a2-macroglobulin-like 1, a protein potentially involved in bacterial immune evasion and bacterial survival. There was increased expression of keratin 6A and interleukin 1b mRNA in bovine digital dermatitis lesions, but reduced expression of most other keratin and keratin-associated genes. There was little evidence of local immune reactions to the bacterial infection present in lesions. Ten samples were processed; five normal skin biopsies from the hind foot skin and five digital dermatitis lesions (large (>2cm) red raw in appearance).

2013-03-26 | E-GEOD-41732 | biostudies-arrayexpress

Differential DNA Methylation Patterns Define Status Epilepticus and Epileptic Tolerance

Project description:Comparison of methylation profiles in the CA3 region of the mouse hippocampus in epileptic tolerance and status epilepticus.

2012-02-09 | E-MEXP-3503 | biostudies-arrayexpress

Epileptic Encephalopathy

Project description:A novel null homozygous mutation confirms CACNA2D2 as a gene mutated in epileptic encephalopathy

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Immune Profiling of Premalignant Lesions in Patients with Lynch Syndrome

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PLCG2 regulates endocannabinoid and eicosanoid networks in innate immune cells

Project description:Human genetic studies have pointed to a prominent role for innate immunity and lipid pathways in human immunological and neurodegenerative disorders. Our understanding of the composition and function of immunomodulatory lipid networks in innate immune cells, however, remains incomplete. Here, we show that phospholipase C gamma 2 (PLCγ2 or PLCG2) – mutations in which are associated with autoinflammatory disorders and Alzheimer’s disease – serves as a principal source of diacylglycerol (DAG) pools that are converted into a cascade of bioactive endocannabinoid (eCB) and eicosanoid lipids by DAG lipase (DAGL) and monoacylglycerol lipase (MGLL) enzymes in innate immune cells. We show that this lipid network is tonically stimulated by disease-relevant human mutations in PLCγ2, as well as Fc receptor activation in primary human and mouse macrophages. Genetic disruption of PLCγ2 in mouse microglia suppressed DAGL/MGLL-mediated eCB-eicosanoid crosstalk and also caused widespread transcriptional and proteomic changes, including the reorganization of immune-relevant lipid pathways reflected in reductions in DAGLB and elevations in PLA2G4A. Despite these changes, Plcg2-/- mice showed generally normal pro-inflammatory cytokine responses to lipopolysaccharide treatment, instead displaying a more restricted deficit in microglial activation that included impairments in prostaglandin production and CD68 expression. Our findings enhance the understanding of PLCγ2 function in innate immune cells, delineating a role in crosstalk with endocannabinoid/eicosanoid pathways and modulation of subsets of cellular responses to inflammatory stimuli.

2021-10-05 | PXD027350 | Pride

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