Figure 8.

Phenotype of CD11b⁺/Ly6C^lo intraspinal macrophages after SCI. Ly6C^lo macrophages were identified by gating on CD11b⁺ events (as in Fig. 5). Subsequently, iNOS, CCR2, MHCII, and CD11c expression was analyzed within the Ly6C^lo gate (one example is shown). Representative histograms of postinjury iNOS, CCR2, MHCII, and CD11c expression are shown for CX3CR1^GFP/GFP (white) and wild-type (shaded) mice. Mean fluorescent intensity is indicated within each representative histogram for each genotype and significant differences are indicated with an asterisk(s). Vertical lines indicate positive expression defined with isotype controls. Quantification of the number of events in the Ly6C^lo/CD11b⁺ gate is graphed below each column. Decreased numbers of iNOS⁺/Ly6C^lo/CD11b⁺ macrophages were found in CX3CR1-deficient mice (effect of genotype was p = 0.0016). The interaction of time and genotype was also significant (p = 0.0057). Conversely, CCR2⁺/Ly6C^lo/CD11b⁺ macrophages were significantly increased in CX3CR1-deficient mice (effect of genotype was p = 0.0006). MHCII⁺/Ly6C^lo/CD11b⁺ macrophages were decreased in CX3CR1-deficient mice (effect of genotype was p = 0.0133). The interaction was also significant (p = 0.0131). The effect of genotype alone on CD11c⁺/Ly6C^lo/CD11b⁺ macrophage numbers was not significant, but there was a significant interaction (p = 0.0473), suggesting that the onset of CD11c⁺ macrophage accumulation is a late occurrence, but still altered by CX3CR1 deletion. Data were analyzed by two-way ANOVA followed by Bonferroni's post hoc test. n = 4 mice/genotype/time. **p < 0.01, ***p < 0.001.