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Increased (18)F-FDG uptake in a model of inflammation: concanavalin A-mediated lymphocyte activation
Takayoshi Ishimori1, Tsuneo Saga, Marcelo Mamede
1Department of Nuclear Medicine and Diagnostic Imaging, Graduate School of Medicine, Kyoto University, Kyoto, Japan. ishimori@kuhp.kyoto-u.ac.jp
Unlabelled:
The aim of this project was to study a mechanism that might explain the increased uptake of (18)F-labeled FDG seen in inflammation. The approach chosen was to examine the effect on (18)F-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 microCi) (18)F-FDG. One hour later, biodistribution was determined. The distribution of the radiolabel in the liver was also evaluated by autoradiography. In vitro (18)F-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 (18)F-FDG (0.74 MBq [20 microCi]/200 microL).
Results:
In immunocompetent BALB/c mice, pretreatment with Con A significantly increased (18)F-FDG uptake in the spleen and liver. Autoradiographs of the liver showed that pretreatment with Con A produced a specific localization of (18)F-FDG at periportal areas, where numerous sites of cellular infiltration were observed. In vitro binding of (18)F-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 (18)F-FDG uptake. Con A-activated lymphocytes actively took up (18)F-FDG both in vitro and in vivo, and (18)F-FDG specifically accumulated in Con A-mediated acute inflammatory tissues.