Fig. 4

Increased microglial reaction after TBI. CX3CR1^+/+ (WT; white bar) and CX3CR1^−/− (KO, black bar) brain leukocytes were analyzed by flow cytometry, and total cellularity, numbers of blood derived infiltrating cells, and CD45^Low microglial cells were compared. a–c After TBI, a significant increase in the overall cellularity was observed when comparing all groups at 15 days (*P < 0.05 comparing sham WT versus WT-TBI 15 days post-TBI), and these changes were sustained 30 days post-TBI. CD45^High hematogenous population did not show statistical significance among injured WT and KO mice. d–f There was a significant increase in microglial cell number at 15 days post-TBI in WT mice when compared to sham WT group. CX3CR1 KO-TBI group also showed a significant increase in microglia number when comparing 15 and 30 days post-TBI, although effects were also seen in the sham-treated KO group. g–i Staining for Ki67 in representative sample of WT-TBI (g upper panel) and KO-TBI (g lower panel) groups and also presented in histogram (h) with gray line showing the isotype controls, WT-TBI Ki67 intensity in blue line, and KO-TBI in red. Data were quantified (i) revealing that in the absence of CX3CR1, microglial cells exhibit a higher proliferative capacity (*P < 0.05)