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Increased ¹⁸F-FDG Uptake in a Model of Inflammation: Concanavalin A-Mediated Lymphocyte Activation

¹ Department of Nuclear Medicine and Diagnostic Imaging, Graduate School of Medicine, Kyoto University, Kyoto, Japan
² Department of Diagnostic and Interventional Imagiology, Graduate School of Medicine, Kyoto University, Kyoto, Japan

The aim of this project was to study a mechanism that might explain the increased uptake of ¹⁸F-labeled FDG seen in inflammation. The approach chosen was to examine the effect on ¹⁸F-FDG uptake of acute activation of murine lymphocytes by concanavalin A (Con A). Methods: Immunocompetent BALB/c mice and nude mice received an intravenous injection of 10 mg/kg Con A. Twenty-four hours later, the mice received an intravenous injection of 0.74 MBq (20 µCi) ¹⁸F-FDG. One hour later, biodistribution was determined. The distribution of the radiolabel in the liver was also evaluated by autoradiography. In vitro ¹⁸F-FDG uptake to splenocytes from BALB/c mice with and without Con A pretreatment were determined 30, 60, and 120 min after the splenocytes were mixed with ¹⁸F-FDG (0.74 MBq [20 µCi]/200 µL). Results: In immunocompetent BALB/c mice, pretreatment with Con A significantly increased ¹⁸F-FDG uptake in the spleen and liver. Autoradiographs of the liver showed that pretreatment with Con A produced a specific localization of ¹⁸F-FDG at periportal areas, where numerous sites of cellular infiltration were observed. In vitro binding of ¹⁸F-FDG to the splenocytes was significantly higher for Con A-pretreated BALB/c mice than for control mice. Conclusion: This study showed that Con A increased ¹⁸F-FDG uptake. Con A-activated lymphocytes actively took up ¹⁸F-FDG both in vitro and in vivo, and ¹⁸F-FDG specifically accumulated in Con A-mediated acute inflammatory tissues.

Key Words: ¹⁸F-FDG PET • concanavalin A • lymphocyte • acute inflammation

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