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Boosting NAD preferentially blunts TH17 inflammation via arginine biosynthesis and redox regulatory control in control and psoriasis subjects [NR or placebo]

ABSTRACT: Boosting NAD preferentially blunts TH17 inflammation via arginine biosynthesis and redox regulatory control in control and psoriasis subjects [NR or placebo]

PROVIDER: PRJNA995628 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25309800_1.fastq.gz	Fastqsanger.gz
	SRR25309800_2.fastq.gz	Fastqsanger.gz
	SRR25309801_1.fastq.gz	Fastqsanger.gz
	SRR25309801_2.fastq.gz	Fastqsanger.gz
	SRR25309802_1.fastq.gz	Fastqsanger.gz

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Boosting NAD preferentially blunts TH17 inflammation via arginine biosynthesis and redox regulatory control in control and psoriasis subjects [NR or placebo]

Project description:To evaluate whether NAD+-boosting modulates adaptive immunity, primary CD4+ T cells from healthy control and psoriasis subjects were exposed to vehicle or nicotinamide riboside (NR) supplementation. NR blunts IFNg and IL-17 secretion with greater effects on TH17 polarization. RNA-seq analysis implicates NR blunting of sequestosome 1 (SQSTM1/p62)-coupled oxidative stress. NR administration increases SQSTM1 and reduces reactive oxygen species (ROS) levels. Furthermore NR activates NRF2, and genetic knockdown of NRF2 and of the NRF2-dependent gene, SQSTM1 diminish NR amelioratory effects. Metabolomic analysis identify that NAD+-boosting increases arginine and fumarate biosynthesis and genetic knockdown of argininosuccinate lyase ameliorates NR-effects on IL-17 production. Hence, NR via amino acid metabolites orchestrate NRF2 activation, augments CD4+ T cell antioxidant defenses and attenuates TH17 responsiveness. Oral NR supplementation in healthy volunteers similarly increase serum arginine, SQSTM1 and antioxidant enzyme gene expression and blunts TH17 immune responsiveness, supporting evaluation of NAD+-boosting in CD4+ T cell linked inflammation.

2023-07-18 | GSE237555 | GEO

Boosting NAD preferentially blunts TH17 inflammation via arginine biosynthesis and redox regulatory control in control and psoriasis subjects [healthy or psoriasis]

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Boosting NAD preferentially blunts TH17 inflammation via arginine biosynthesis and redox regulatory control in control and psoriasis subjects

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Boosting NAD preferentially blunts TH17 inflammation via arginine biosynthesis and redox regulatory control in control and psoriasis subjects [healthy or psoriasis]

Project description:Boosting NAD preferentially blunts TH17 inflammation via arginine biosynthesis and redox regulatory control in control and psoriasis subjects [healthy or psoriasis]

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Boosting NAD+ blunts toll-like receptor-4 induced type I interferon in control and systemic lupus erythematosus monocytes

Project description:This is a pilot study to evaluate the effects of NR supplementation on monocytes function, registered in ClinicalTrials.gov with registration number: NCT02812238 and approved by the National Heart and Lung Institute IRB.

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Boosting NAD preferentially blunts TH17 inflammation via arginine biosynthesis and redox regulatory control in control and psoriasis subjects

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