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Disulfiram inhibits neutrophil extracellular trap formation and protects rodents during acute lung injury and SARS-CoV-2 infection

ABSTRACT: Disulfiram inhibits neutrophil extracellular trap formation and protects rodents during acute lung injury and SARS-CoV-2 infection

PROVIDER: PRJNA748088 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15194710.fastq.gz	Fastqsanger.gz
	SRR15194711.fastq.gz	Fastqsanger.gz
	SRR15194712.fastq.gz	Fastqsanger.gz
	SRR15194713.fastq.gz	Fastqsanger.gz
	SRR15194714.fastq.gz	Fastqsanger.gz

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Disulfiram inhibits neutrophil extracellular trap formation and protects rodents during acute lung injury and SARS-CoV-2 infection

Project description:Assess the ability of disulfiram to inhibit NET formation and improve disease outcome in a Syrian hamster model of COVID-19. RNA sequencing was performed Golden Syrian hamster lung inoculated with SARS-CoV-2 in PBS or PBS only and treated with disulfiram or vehicle control sesame oil with dexamethasone.

2022-04-11 | GSE180417 | GEO

Disulfiram inhibits neutrophil extracellular trap formation and protects rodents from acute lung injury and SARS-CoV-2 infection.

Project description: Not available

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Dysregulated neutrophil responses and neutrophil extracellular trap formation and degradation in PAPA syndrome

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FDA-approved Disulfiram Inhibits the NLRP3 Inflammasome

Project description:The NLRP3 inflammasome is dysregulated in autoinflammatory disorders caused by inherited mutations and contributes to the pathogenesis of several chronic inflammatory diseases. In this study, we discovered that disulfiram, a safe FDA-approved drug, specifically inhibits the NLRP3 inflammasome, but not the NLRC4 or AIM2 inflammasomes. Disulfiram suppresses caspase-1 activation, ASC speck formation, and pyroptosis induced by several stimuli that activate NLRP3. Mechanistically, NLRP3 is palmitoylated at cysteine 126, a modification required for its localization to the trans-Golgi network and inflammasome activation which was inhibited by disulfiram. Administration of disulfiram to animals inhibited the NLRP3, but not the NLRC4 inflammasome in vivo. Our study uncovers a mechanism by which disulfiram targets NLRP3 and provides a rationale for using a safe FDA-approved drug for the treatment of NLRP3-associated inflammatory diseases.

2024-07-25 | PXD054126 | Pride

Intralipid protects the heart in late pregnancy against ischemia/reperfusion injury

Project description:The heart of late pregnant (LP) rodents is more prone to ischemia/reperfusion (I/R) injury compared to non-pregnant rodents. We hypothesized that Intralipid (ITLD) protects the heart in LP rodents against I/R injury. We performed genome-wide expression profiling to identify the underlying mechanisms. Female LP rat hearts were subjected to ischemia followed by reperfusion with vehicle or ITLD (one bolus of 5mg/kg).

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Disulfiram inhibits bacterial growth by inducing zinc-dependent reactive oxygen species

Project description:With the growing threat posed by emerging drug-resistant bacteria, the discovery of new antibiotics and the exploration of additional antimicrobial mechanisms of medicines currently used in the clinic are urgent. In this study, we found that disulfiram, a drug used for the treatment of alcohol addiction, inhibited the growth of multiple bacteria and quickly inhibited the growth of E. coli. When combined with kanamycin or polymyxins in vitro, disulfiram could augment the bactericidal effect against E. coli or A. baumannii. When combined with colistin in vivo, disulfiram also protected against murine E. coli infection. Disulfiram inhibited the motility of E. coli but did not change its length morphologically. Transcriptomic analysis revealed that disulfiram-treated E. coli presented an oxidative stress pattern and zinc-related transcriptomic changes. Moreover, the bacteriostatic effect of disulfiram on E. coli and S. aureus could be fully prevented by the ROS scavenger NAC. In addition, zinc ions increased ROS levels and further suppressed bacterial growth, whereas zinc chelators suppressed ROS and restored the growth of both E. coli and S. aureus. This study reveals that disulfiram inhibits bacterial growth by inducing zinc-dependent intracellular reactive oxygen species (ROS). This bacteriostatic effect can be reversed by ROS scavengers or zinc chelators, highlighting a previously uncharacterized antimicrobial mechanism for disulfiram.

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Intralipid protects the heart in late pregnancy against ischemia/reperfusion injury

2016-02-09 | GSE77698 | GEO

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