Abstract
Abstract NAD +-boosting via nicotinamide riboside (NR) confer anti-inflammatory effects. However, underlying mechanisms and therapeutic potential remain incompletely defined. Given NAD +is a co-enzyme in oxidoreductive reactions, metabolomics analysis identified two major metabolites that were increased by NR: inosine and Prostaglandin E2 (PGE2). Both inosine and PGE2 supplementation blunted IFNβ release, however NR-mediated monocytic downregulation of IFNβ was dependent on inosine but independent of PGE2. Flow cytometric analysis of cell surface receptors in human M1 macrophage showed NR increased the expression of CC-chemokine receptor 7 (CCR7). Consequently, chemokine ligand 19 (CCL19, ligand for CCR7) - induced macrophage migration was enhanced in response to NR administration. Furthermore, NR-mediated upregulation of macrophage migration through CCL19-CCR7 axis was dependent on PGE2 synthesis. We also demonstrated that NR upregulates PGE2 synthesis through Sirt1-dependent transcriptional regulation of COX2. NR-mediated metabolic regulation appears to modulate disparate myeloid cell functions via distinct signaling intermediates and pathways. NHLBI Division of Intramural Research
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