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

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

PROVIDER: PRJNA791901 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17320000_1.fastq.gz	Fastqsanger.gz
	SRR17320000_2.fastq.gz	Fastqsanger.gz
	SRR17320001_1.fastq.gz	Fastqsanger.gz
	SRR17320001_2.fastq.gz	Fastqsanger.gz
	SRR17320002_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.

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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]

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

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

| PRJNA995626 | ENA

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.

2021-12-30 | GSE192536 | GEO

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]

| PRJNA995627 | ENA

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

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

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Boosting NAD+ blunts TLR4-induced type I IFN in control and systemic lupus erythematosus monocytes.

Project description:BACKGROUNDFasting and NAD+-boosting compounds, including NAD+ precursor nicotinamide riboside (NR), confer antiinflammatory effects. However, the underlying mechanisms and therapeutic potential are incompletely defined.METHODSWe explored the underlying biology in myeloid cells from healthy volunteers following in vivo placebo or NR administration and subsequently tested the findings in vitro in monocytes extracted from patients with systemic lupus erythematosus (SLE).RESULTSRNA-Seq of unstimulated and LPS-activated monocytes implicated NR in the regulation of autophagy and type I IFN signaling. In primary monocytes, NR blunted LPS-induced IFN-β production, and genetic or pharmacological disruption of autophagy phenocopied this effect. Given that NAD+ is a coenzyme in oxidoreductive reactions, metabolomics was performed and identified that NR increased the inosine level. Inosine supplementation similarly blunted autophagy and IFN-β release. Finally, because SLE exhibits type I IFN dysregulation, we assessed the NR effect on monocytes from patients with SLE and found that NR reduced autophagy and IFN-β release.CONCLUSIONWe conclude that NR, in an NAD+-dependent manner and in part via inosine signaling, mediated suppression of autophagy and attenuated type I IFN in myeloid cells, and we identified NR as a potential adjunct for SLE management.TRIAL REGISTRATIONClinicalTrials.gov registration numbers NCT02812238, NCT00001846, and NCT00001372.FUNDINGThis work was supported by the NHLBI and NIAMS Intramural Research divisions.

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Bacteria boost mammalian host NAD metabolism by engaging the deamidated biosynthesis pathway

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2021-01-28 | E-MTAB-9449 | biostudies-arrayexpress

Akkermansia muciniphila blunts Th17 cells

Project description:Akkermansia muciniphila blunts Th17 cells

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