Fig. 6. Forced turnover of microglia in aged mice decreases sensitivity to TBI.

(A) Timeline of experimental design immediately before sham and TBI surgery. (B) Representative dot plots of immune populations in the ipsilateral brain hemisphere at 3 days after TBI. Quantification of CD45^intCD11b⁺ microglia and CD45^hiCD11b⁺-infiltrating myeloid cell counts per hemisphere are shown for aged, surgery, and treatment groups. (C) A representative histogram of DHR123⁺ microglia is shown next to the relative MFI quantification of ROS production. In the associated histogram, young groups are shown with no outline, old groups are shown with bold outlines, and treatment groups are color-coded according to bar graph and figure legend (Veh in red and PLX5622 in blue). A vertical fiducial line is included for reference. Representative dot plots depicting (D) IL-1β production and (E) p16 expression in microglia are shown next to quantification of cell frequencies. (F) Cytokine protein concentrations in the peri-lesional cortex as measured by ELISA. No differences were seen between sham control groups after treatment, and so data for both sham groups were combined. For all cytokines (M-CSF, G-CSF, eotaxin, IL-1a, MIG, and MIP-2), TBI acutely increased concentrations in Veh but not PLX5622-treated groups. N = 3 to 4 per sham and 6 to 7 per TBI group. ns, not significant. Data were analyzed using two-way ANOVA with Tukey post hoc correction (B to E) and one-way ANOVA with Bonferroni post hoc correction (F) for multiple comparisons (*P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001).