Fig. 2From: Neuronal CCL2 expression drives inflammatory monocyte infiltration into the brain during acute virus infectionCCL2 levels in serum, whole brain, and hippocampus during acute infection. Serum (a), whole brain (b), and microdissected hippocampus (c) were collected at 0, 3, 6, 12, and 24 h following intracranial inoculation with TMEV. Absolute levels of CCL2 were measured by ELISA. Each dot represents an individual animal. The bar graph shows mean ± 95% confidence intervals from aggregate data. A minimum of three mice were used per tissue per timepoint, and the hippocampal samples were collected in a separate experiment from the whole brain samples. All results were analyzed by one-way ANOVA. CCL2 was induced in serum, whole brain, and hippocampus (P < 0.001 for each factor in each tissue compared to 0 hpi). Brain sections collected at 0 (d, g), 6 (e, h), and 24 hpi (f, i) were immunostained to reveal CCL2 expression. In the hippocampus, there was weak, diffuse signal in uninfected mice (d, g) that increased markedly at 6 hpi (e, h). By 24 hpi, the signal intensity had decreased and exhibited a more punctate pattern (f, i). Scale bar in i is 50 μm and refers to g–i. CA1 cornu ammonis 1 formation, sr stratum radiatum, slm stratum lacunosum moleculare. Immunostaining is representative of more than three mice per timepoint in more than three separate experimentsBack to article page