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Fig. 1 | Journal of Neuroinflammation

Fig. 1

From: A novel interaction between CX3CR1 and CCR2 signalling in monocytes constitutes an underlying mechanism for persistent vincristine-induced pain

Fig. 1

CCR2-deficient mice have reduced VCR allodynia and monocyte infiltration in the sciatic nerve during the second cycle. a Mechanical thresholds are significantly higher in VCR-treated CCR2-deficient (RFP/RFP) mice than heterozygous controls during the second cycle (days 8–11). Data expressed as 50% paw withdrawal thresholds (mean ± SEM, n = 8 mice per group). *p < 0.05 and **p < 0.01 compared to time-matched VCR-treated CCR2+/RFP thresholds, two-way RM ANOVA, post hoc Tukey’s test. b Representative images showing macrophages (F4/80, green) in longitudinal sections of sciatic nerves of CCR2+/RFP and CCR2RFP/RFP mice during both VCR cycles. Scale bar = 200 μm. c Quantification of F4/80 immunoreactive (+) profiles per 104 μm2 (mean ± SEM, n = 4 mice per group; five fields of view were quantified for each mouse). There is a significant reduction in F4/80+ profiles in CCR2RFP/RFP sciatic nerves in cycle 2, relative to CCR2RFP/RFP sciatic nerves during cycle 1 and relative to CCR2+/RFP during cycle 2. *p < 0.05, one-way ANOVA, Tukey’s test. d Representative blot of F4/80 (130 kDa) and α-tubulin loading control (50 kDa) in sciatic nerve homogenates obtained from CCR2+/RFP and CCR2RFP/RFP mice during VCR cycles 1 and 2. e Quantification of F4/80 band density normalised to α-tubulin (mean ± SEM, n = 3). F4/80 expression is unchanged in CCR2+/RFP sciatic nerve homogenates between VCR cycles 1 and 2. In CCR2RFP/RFP sciatic nerve homogenates, there is a significant reduction in normalised F4/80 expression in cycle 2 (day 11) relative to cycle 1 (day 4). *p < 0.05, one-way ANOVA, Tukey’s test

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