Intestinal GVHD in mice after allogeneic HSCT was associated with increased local FDG uptake mainly localized to the colon. Lethally irradiated CB6F1 mice received 2.0 × 107 BMCs alone (allogeneic control; □) or together with 1.0 × 107 splenocytes (allogeneic GvHD group; ●) from parental BALB/c donors. In the syngeneic control group, CB6F1 recipients were given transplanted of grafts from CB6F1 mice containing 2.0 × 107 BMCs and 1.0 × 107 splenocytes (◇). Body weight loss was used as a measure of GVHD in recipient mice after syngeneic (A) or allogeneic (B,C,P) HSCT. In vivo imaging after application of 10 MBq FDG with a small-animal PET scanner 21 days after transplantation (D-I) demonstrated a marked increase of FDG uptake in the colons of animals with GVHD (F,I) compared with physiologic FDG uptake in the gut of both control groups (panels D,G and E,H). Histopathology of the colon revealed GVHD with tissue infiltration by lymphocytes and mucosa cell apoptosis in the GVHD group (L) and no evidence of GVHD in control animals (J,K). In the small intestine of recipient mice with or without GVHD, only low levels of FDG uptake were observed. Histopathologic analyses of the small intestine showed normal mucosa in all groups (M-O). In an independent set of experiments, intensity and progression of GVHD were correlated with FDG-PET results. GVHD severity was monitored using a clinical score (Q), as detailed in “Methods,” and by body weight loss (P). At each time point, 4 to 6 transplant recipients per group were examined in vivo by PET scan 1 hour after application of 10 MBq FDG. FDG uptake associated with gastrointestinal inflammation was quantified by calculation of FDG uptake in the gut as percentage of the dose injected (R). The results are representative of at least 3 independent experiments. Original magnification for histopathology was 100-fold. Error bars indicate positive standard deviations for each time point. *Statistically significant differences versus both control groups (P < .05).
