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Augmented ¹⁸F-FDG Uptake in Activated Monocytes Occurs During the Priming Process and Involves Tyrosine Kinases and Protein Kinase C

Department of Nuclear Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea

Activated monocytes with a high ¹⁸F-FDG accumulation can affect the results of clinical PET studies. To better understand the mechanisms regulating monocytic ¹⁸F-FDG uptake, we investigated the effect of priming and respiratory-burst generation and further evaluated the role of potential protein kinase pathways. Methods: Purified human monocytes were primed with interferon- (IFN-), and respiratory burst was generated by stimulation of primed cells with phorbol-12-myristate-13-acetate (PMA). Oxygen-intermediate generation was assessed by luminescence measurements after the addition of lucigenin. ¹⁸F-FDG uptake after 30 min of incubation was measured for unprimed control cells, primed cells, and PMA-stimulated cells. The role of protein kinases was investigated using respective inhibitors. Results: PMA stimulation of primed monocytes dramatically increased oxygen-intermediate generation, leading to a 42.2 ± 1.1 fold higher level of cumulative luminescence compared with unprimed control cells, whereas IFN- priming alone resulted in low luminescence levels (13.9% ± 4.6% of PMA-stimulated cells). In contrast, priming alone was sufficient to augment monocytic ¹⁸F-FDG uptake to 273.3% ± 16.7% of control levels (P < 0.001), and it was not further increased by PMA stimulation. The tyrosine kinase inhibitor, genistein, and the specific protein kinase C inhibitor, staurosporine, completely abolished the priming-induced enhancement of ¹⁸F-FDG uptake and lowered uptake to control levels. Under the same conditions, wortmannin, a phosphatidylinositol 3 kinase (PI3 kinase)-specific inhibitor, and cycloheximide, a protein synthesis inhibitor, were associated with only minor reductions in the enhanced-uptake effect of priming. Conclusion: IFN- priming alone, without stimulation of respiratory-burst activity, is sufficient to induce maximal augmentation of ¹⁸F-FDG uptake in monocytes. Furthermore, this metabolic effect appears to involve tyrosine kinases and the protein kinase C pathway but is independent of the PI3 kinase pathway.

Key Words: ¹⁸F-FDG • PET • monocytes • interferon- • priming • respiratory burst

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