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Adherence Affects Monocyte Innate Immune Function and Metabolic Reprogramming after Lipopolysaccharide Stimulation In
Natasja A Otto1,2, Joe M Butler3,2, Ivan Ramirez-Moral3,2
1Center for Experimental and Molecular Medicine, University of Amsterdam, 1105 AZ Amsterdam, the Netherlands; n.a.otto@amsterdamumc.nl.
Journal of Immunology (Baltimore, Md. : 1950)
|January 7, 2021
Summary
Monocyte adherence alters immune responses, promoting anti-inflammatory and phagocytic functions. Inhibiting both glycolysis and oxidative phosphorylation, but not glycolysis alone, profoundly impacts monocyte immune functions during LPS stimulation.
Area of Science:
- Immunology
- Cell Biology
- Metabolism
Background:
- Monocytes are crucial immune cells that differentiate into macrophages in tissues.
- Cellular metabolism significantly influences immune cell function and phenotype.
- Adherence is a key step in monocyte migration and activation.
Purpose of the Study:
- To investigate the impact of adherence on human monocyte metabolic and functional responses to LPS.
- To elucidate the role of glycolysis and oxidative phosphorylation in LPS-stimulated monocyte immune functions.
Main Methods:
- Human monocytes were stimulated with LPS under nonadherent and adherent conditions.
- Monocyte cytokine production, phagocytosis, and reactive oxygen species generation were assessed.
- RNA sequencing, gene set enrichment, and [13C]-glucose flux analysis were employed.
- Glycolysis was inhibited using glucose deprivation or 2-deoxy-d-glucose (2DG).
Main Results:
- Adherent monocytes produced less pro-inflammatory cytokines (TNF, IL-1β) and more anti-inflammatory IL-10 upon LPS stimulation.
- Adherence enhanced monocyte phagocytosis and reactive oxygen species production.
- Adherence modulated LPS-induced gene expression, favoring pathogen elimination pathways.
- 2DG, unlike glucose deprivation, inhibited TLR signaling, pathogen elimination genes, and cytokine release, and reduced oxidative phosphorylation gene expression.
Conclusions:
- Monocyte adherence alters their metabolic profile, increasing glycolysis.
- Inhibition of both glycolysis and oxidative phosphorylation is required to significantly impact LPS-induced monocyte immune functions.
- Metabolic reprogramming, particularly involving oxidative phosphorylation, plays a critical role in monocyte immune responses.
