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IL-10 prevents pathological microglia hyperactivation following peripheral endotoxin challenge

ABSTRACT: IL-10 prevents pathological microglia hyperactivation following peripheral endotoxin challenge

PROVIDER: PRJNA661455 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12588807_1.fastq.gz	Fastqsanger.gz
	SRR12588807_2.fastq.gz	Fastqsanger.gz
	SRR12588808_1.fastq.gz	Fastqsanger.gz
	SRR12588808_2.fastq.gz	Fastqsanger.gz
	SRR12588809_1.fastq.gz	Fastqsanger.gz

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IL-10 prevents pathological microglia hyperactivation following peripheral endotoxin challenge

Project description:Microglia, the resident macrophages of the brain parenchyma, are central players in CNS development, homeostasis and disorders. Distinct brain pathologies seem associated with discrete microglia activation modules. How microglia regain their ground state following challenges remains much less understood. Here, we explored the role of the IL-10 axis in restoring murine microglia homeostasis following peripheral endotoxin challenge. Specifically, we show that lipopolysaccharide (LPS)-challenged mice harboring IL-10 receptor-deficient microglia display neuronal impairment and succumb to fatal sickness. Addition of a microglial TNF deficiency rescues these animals, suggesting a microglia-based circuit driving pathology. Single cell transcriptome analysis revealed various IL-10 producing resident and recruited immune cell in the CNS, including most prominently Ly49D+ NK cells and neutrophils, but not microglia. Collectively, we define the kinetics of the microglia response to peripheral endotoxin challenge, including their activation and robust silencing, and highlight the critical role of non-microglial IL-10 in preventing deleterious microglia hyperactivation.

2020-10-22 | GSE157480 | GEO

Neural transcriptomic responses to endotoxin challenge across social treatments

Project description:The aim of this experiment was to test whether the social setting changed neural transcriptomic responses to an endotoxin challenge in zebra finches

2023-03-06 | GSE203528 | GEO

Gene expression Profiling of Peripheral Blood Leukocytes after Endotoxin Challenge in Humans

Project description:Peripheral blood mononuclear cells were isolated 0, 30 min, 6 h, 24 h, and 7 day after intravenous endotoxin challenge. Keywords: time course

2006-01-17 | GSE3026 | GEO

Neural transcriptomic responses to endotoxin challenge across social treatments

Project description:Neural transcriptomic responses to endotoxin challenge across social treatments

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Mouse kidney after systemic endotoxin challenge

Project description:8 week-old male C57BL6J mice were given Gram-negative endotoxin (LPS O111:B4, 10 mg/kg) intraperitoneally at time 0. 18 hrs thereafter, they were administered 10 ml/kg 0.9% saline. Mice were sacrificed at 0, 18, or 42 hrs after LPS challenge. Kidneys were immediately collected into TRIzol for RNA preparation. Renal function was measured on blood collected at the time of tissue harvest At t=0hr, mice had normal baseline renal function. At t=18hr, mice exhibited early renal injury, At t=42hr, mice had either recovered normal renal function or had persistent renal injury. We collected kidneys from 3 mice per time point. For the 42 hr time point, we collected kidneys from 3 mice with recovered renal function and kidneys from 3 mice with persistent renal injury. Mouse kidneys selected at successive stages of renal injury and recovery following systemic LPS challenge and volume resuscitation following LPS challenge.

2011-07-12 | E-GEOD-30576 | biostudies-arrayexpress

A cyanobacterial LPS antagonist prevents endotoxin shock and blocks sustained TLR4 stimulation

Project description:A cyanobacterial LPS antagonist prevents endotoxin shock and blocks sustained TLR4 stimulation required for cytokine expression. We report the identification and biologic characterization of an LPS-like molecule extracted from the cyanobacterium Oscillatoria Planktothrix FP1 (CyP). Keywords: different ligands

2006-07-27 | GSE4748 | GEO

Mouse kidney after systemic endotoxin challenge

2011-07-12 | GSE30576 | GEO

Expression data from from NOS2-deficient (NOS2-/-) and wild-type mice subjected to endotoxin or saline challenge

Project description:Hypoxic pulmonary vasoconstriction (HPV) optimizes the match between ventilation and perfusion in the lung by reducing blood flow to poorly ventilated regions. Sepsis and endotoxemia impair HPV. We previously showed that nitric oxide synthase 2 (NOS2) is required, but not sufficient, for the effect of endotoxin on HPV. The aim of the current study was to identify additional factors that might contribute to the impairment of HPV during endotoxemia. Microarray gene expression profiling was determined using pulmonary tissues from NOS2-deficient (NOS2-/-) and wild-type mice subjected to endotoxin (LPS) or saline challenge (control).

2019-05-09 | GSE130936 | GEO

Transcription profiling of human dendritic monocytes treated with LPS (lipopolysaccharide) or CyP (Cyanobacterial Product) reveals cyanobacterial LPS antagonist prevents endotoxin shock and blocks sustained TLR4 stimulation required for cytokine expression

2007-10-26 | E-GEOD-4748 | biostudies-arrayexpress

Morphine induced sepsis is mediated by abrogation of endotoxin tolerance through modulation of miR-146a, but not miR-155.

Project description:Endotoxin/LPS tolerance is a tightly regulated phenomenon, which, during infection, prevents systemic hyper-inflammation. Here we report for the first time that morphine reversal of endotoxin tolerance resulting in persistent inflammation thus contributing to septicemia and septic shock. We further report that this regulation is mediated by LPS-induced down-regulation of microRNAs 146a and 155. However, only over-expression of miR-146a, but not miR-155 abrogates morphine mediated hyper-inflammation, while antagonizing miR-146a (but not miR-155) augments morphine mediated hyper-inflammation. Hence, miR-146a could be the potential therapeutic target for morphine-mediated abrogation of endotoxin tolerance.

2013-08-01 | GSE42506 | GEO

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