Figure 1. Diffuse TBI promoted neuroinflammation in mice in a time-dependent manner.

Four or 72 h after sham operation or TBI, mRNA levels of IL-1β, CD14, and TNFα were determined in the CX and underlying HPC (n=6–9), or enriched brain CD11b⁺ cells were collected and CD11b, CD45, and CD14 surface expression was determined by flow cytometry (n=3–5). A) There was a main effect of TBI on IL-1β expression in both the CX (F(2,21=11.01, p<0.0007) and HPC (F(2,22)=28.22, p<0.0006). B) There was a main effect of TBI on CD14 expression in both the CX (F(2,20)=33.23, p<0.0001) and HPC (F(2,19)=22.22, p<0.0001) and CD14 remained elevated in the HPC 72 h after TBI (p<0.0002). C) There was a main effect of TBI on TNFα in both the CX (F(2,20)=32.00, p<0.0001) and HPC (F(2,21)=284.89, p<0.0001). D) Representative bivariate dot plots of CD11b/CD45 staining of enriched brain CD11b⁺ cells. E) TBI increased the relative number of PMCs (CD11b⁺/CD45^high) associated with the brain both 4 and 72 h after injury (F(2,12)=34.37, p<0.006). F) Representative bivariate dot plots of CD11b/CD14 staining on microglia (CD11b⁺/CD45^low). G) TBI increased the percent of CD14^high microglia present 4 and 72 h after injury (F(2,10)=28.23, p<0.01). Bars represent the mean ± SEM. Means with (*) are significantly different (p<0.05) from sham controls. Means with (#) are significantly different (p<0.05) from sham control and TBI-4h groups. CX = cortex; HPC = hippocampus.