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Fig. 5 | Journal of Neuroinflammation

Fig. 5

From: Neuronal CCL2 expression drives inflammatory monocyte infiltration into the brain during acute virus infection

Fig. 5

Neurons are the primary source of CCL2 at 6 hpi. Ccl2-RFPfl/fl reporter mice (ac) and Syn-Cre x Ccl2-RFPfl/fl neuron-specific CCL2-deficient mice (df) were intracranially inoculated with TMEV and brain sections were collected at 6 hpi for analysis of RFP expression. Single-channel RFP (a, d) and two-channel RFP (red) and DAPI (blue) (b, e) microscopy revealed that the reporter signal present in neurons at 6 hpi was specifically deleted in the Syn-Cre x Ccl2-RFPfl/fl mice. Higher power imaging of the CA1 pyramidal neuron layer verified the presence of reporter signal (red) in these neurons (marked by DAPI; white) in Ccl2-RFPfl/fl mice (c) and the almost complete absence of such signal in the conditional knockout (f). Immunostaining with anti-CCL2 antibody confirmed the presence of CCL2 (green) in CA1 neurons (marked by DAPI; blue) and in the stratum lacunosum moleculare at 6 hpi in Ccl2-RFPfl/fl mice (g) and the absence of CCL2 in the hippocampus of Syn-Cre x Ccl2-RFPfl/fl conditional knockout mice (h). Serum (i) and hippocampal (j) CCL2 levels were measured by ELISA at 0, 6, and 24 hpi in the CCL2 reporter mice (+CCL2) and the neuron-specific CCL2-deficient mice (−CCL2). Each dot represents one animal; bar graphs represent mean ± 95%CI calculated from at least three mice per group per timepoint. Data were analyzed by two-way ANOVA with Tukey-Kramer pairwise analysis; statistical significance is only shown between genotypes at each timepoint; **P < 0.001; ***P < 0.0001. CA1 cornu ammonis 1 formation, sr stratum radiatum, slm stratum lacunosum moleculare. Fluorescence in af is representative of more than three mice in two separate experiments; immunostaining in gh is representative of two animals in each group

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