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Inhibition of netosis with PAD inhibitor attenuates endotoxin shock induced systemic inflammation

ABSTRACT: Inhibition of netosis with PAD inhibitor attenuates endotoxin shock induced systemic inflammation

PROVIDER: PRJNA839858 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19346552_1.fastq.gz	Fastqsanger.gz
	SRR19346552_2.fastq.gz	Fastqsanger.gz
	SRR19346553_1.fastq.gz	Fastqsanger.gz
	SRR19346553_2.fastq.gz	Fastqsanger.gz
	SRR19346554_1.fastq.gz	Fastqsanger.gz

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Inhibition of netosis with PAD inhibitor attenuates endotoxin shock induced systemic inflammation

Project description:Neutrophils play a pivotal role in innate immunity and participate in a range of immunological disorders. Excessive neutrophil extracellular traps formed at infection and tissue damage sites are detrimental to the local tissue and further exacerbate inflammation. Protein arginine deiminases mediate histone citrullination and NET formation thereby regulating endotoxin shock response. However, the molecular mechanisms are less known. Here we report that inhibition of netosis attenuates inflammation in a LPS induced lethal endotoxic shock model in mice. Albeit a higher number of neutrophils are accumulated in peritoneal cavity the primary inflammatory site, the level of inflammatory signals is greatly reduced after netosis inhibition with a PAD inhibitor. In lungs under endotoxic stress, gene expression analyses indicate that LPS induced a drastic increase in inflammatory gene expression. In contrast, lung tissue damage and inflammation were much reduced after PAD inhibition to reduce netosis. In summary, we found NET formation inhibition as a new avenue to manage inflammatory damages under endotoxic stress.

2022-12-01 | GSE203340 | GEO

Inhibition of Netosis with PAD Inhibitor Attenuates Endotoxin Shock Induced Systemic Inflammation.

Project description:Neutrophils play a pivotal role in innate immunity by releasing neutrophils extracellular traps (NETs). Excessive NETs are detrimental to the local tissue and further exacerbate inflammation. Protein arginine deiminases (PAD) mediate histone citrullination and NET formation that, in turn, exacerbate endotoxin shock damages. In this study, we further investigated the molecular mechanism underlying PAD and NETs in endotoxic stress in mice. The control group mice were injected with solvent, the LPS endotoxic shock group mice were intraperitoneally injected with LPS at 35 mg/kg only, while the LPS and PAD inhibitor YW3-56 treatment group mice were injected with YW3-56 at 10 mg/kg prior to the LPS injection. YW3-56 significantly prolonged the survival time of the LPS-treated mice. NETs, cfDNA, and inflammatory factors were detected by ELISA in serum, paitoneal cavity, and lung at 24 h after LPS administration. Lung injuries were detected by immunostaining, and lung tissue transcriptomes were analyzed by RNA-seq at 24 h after LPS administration. We found that YW3-56 altered neutrophil tissue homeostasis, inhibited NET formation, and significantly decreased cytokines (IL-6, TNFα and IL-1β) levels, cytokines gene expression, and lung tissue injury. In summary, NET formation inhibition offers a new avenue to manage inflammatory damages under endotoxic stress.

| S-EPMC9655899 | biostudies-literature

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

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

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

2013-08-01 | E-GEOD-42506 | biostudies-arrayexpress

Mouse kidney endotoxin time course

Project description:Time course of endotoxin-induced acute kidney injury in mice

2023-11-15 | GSE247727 | GEO

Tamm-Horsfall protein augments neutrophil NETosis

Project description:Proteome profiles of isolated peripheral human neutrophils pretreated with purified Tamm-Horsfall protein and stimulated to undergo NETosis with PMA.

2024-09-23 | PXD045468 | Pride

IDENTIFICATION OF BIOMARKERS OF RESPONSE TO IFNG DURING ENDOTOXIN TOLERANCE: APPLICATION TO SEPTIC SHOCK

Project description:The rapid development in septic patients of features of marked immunosuppression associated with increased risk of nosocomial infections and mortality represents the rational for the initiation of immune targeted treatments in sepsis. However, as there is no clinical sign of immune dysfunctions, the current challenge is to develop biomarkers that will help clinicians identify the patients that would benefit from immunotherapy and monitor its efficacy. Using an in vitro model of endotoxin tolerance (ET), a pivotal feature of sepsis-induced immunosuppression in monocytes, we identified using gene expression profiling by microarray a panel of transcripts associated with the development of ET which expression was restored after immunostimulation with interferon-gamma (IFN-γ). These results were confirmed by qRT-PCR. Importantly, this short-list of markers was further evaluated in patients. Of these transcripts, six (TNFAIP6, FCN1, CXCL10, GBP1, CXCL5 and PID1) were differentially expressed in septic shock patients’ blood compared to healthy blood upon ex vivo LPS stimulation and were restored by IFN-γ. In this study, by combining a microarray approach in an in vitro model and a validation in clinical samples, we identified a panel of six transcripts that could be used for the identification of septic patients eligible for IFNg therapy. The potential value of these markers should now be evaluated in a larger cohort of patients. Upon favorable results, they could serve as stratification tools prior to immunostimulatory treatment and to monitor drug efficacy.

2013-07-31 | GSE46914 | GEO

Mouse kidney endotoxin time course

Project description:Mouse kidney endotoxin time course

| PRJNA1040219 | ENA