Fig. 6

Loss of acute neuronal CCL2 production results in reduced inflammatory monocyte infiltration into the brain. Brain-infiltrating leukocytes were analyzed by flow cytometry in wildtype B6 mice (a), Ccl2-RFP^fl/fl reporter mice (+CCL2; b), and Syn-Cre x Ccl2-RFP^fl/fl neuron-specific CCL2-deficient mice (−CCL2; c) at 18 hpi. The flow plots in (a–c) show Gr1- and CD11b-labeled cells in a CD45^hi parent gate. The number of CD45^hi cells (d), neutrophils (e), and inflammatory monocytes (f) were counted in the three groups (blue circles = B6; black circles = +CCL2; red circles = −CCL2). Each dot represents one animal; the line graph represents mean ± 95%CI calculated from at least two separate experiments. All cell types were significantly reduced in the neuron-specific CCL2-deficient mice but not in the parent reporter line. Data were analyzed by one-way ANOVA with Dunnett’s pairwise comparison; *P ≤ 0.0001