Exploratory experiment designed to discover new patterns targeting NAMPT in Primary mouse and human monocytes/macrophages. Primary outcome: Macrophage polarization markers and cytokine production
In vitro investigation of how NAD depletion affects the differentiation and polarization of primary monocytes and macrophages from both mouse and human sources. The experiment examined the impact of FK866-mediated NAD depletion on macrophage biology, specifically focusing on how reduced NAD availability influences macrophage polarization states. Results showed that NAD depletion skewed macrophage polarization toward an anti-inflammatory phenotype, with reduced expression of pro-inflammatory markers (CD86, CD38, MHC-II, IL-6) and increased expression of anti-inflammatory markers (CD206, Egr2, IL-10). This mechanistic study provided crucial insights into how NAD metabolism directly regulates immune cell function.
Isolation of primary monocytes/macrophages, FK866 treatment, assessment of differentiation markers and cytokine profiles
Altered macrophage polarization with reduced pro-inflammatory and increased anti-inflammatory markers
Significant changes in polarization markers (CD86, CD38, MHC-II, IL-6 reduction; CD206, Egr2, IL-10 increase)
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