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Fig. 2 | Journal of Neuroinflammation

Fig. 2

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

Fig. 2

RS-102895 significantly reduces VCR-induced allodynia and monocyte infiltration in the sciatic nerve in CX3CR1-deficient mice. a CX3CR1 knockout (GFP/GFP) mice were treated with two VCR cycles alongside the CCR2 antagonist RS-102985, or vehicle, during the VCR cycle 2. CX3CR1GFP/GFP mice developed VCR-induced allodynia at the end of cycle 1 (day 4) as previously reported. Data expressed as 50% paw withdrawal thresholds (mean ± SEM, n = 6–9 mice per group). In VCR/RS-102895-treated CX3CR1GFP/GFP mice (red trace), withdrawal thresholds increased significantly relative to VCR/vehicle-treated CX3CR1GFP/GFP mice (blue) within 24 h of the first antagonist dose. *p < 0.05, two-way RM ANOVA, Tukey’s test. b Representative images of macrophages (F4/80, red) in sciatic nerve longitudinal sections at day 11 from VCR-treated CX3CR1GFP/GFP and CX3CR1+/GFP mice. Scale bar = 50 μm. c Quantification of F4/80+ profiles per 104 μm2 in the sciatic nerve at day 11 (mean ± SEM, n = 4 mice per group; five fields of view were quantified for each mouse). RS-102985 significantly reduces VCR-induced elevation of F4/80+ profiles in sciatic nerves from CX3CR1GFP/GFP mice. NS not significant, **p < 0.01, one-way ANOVA, Tukey’s test. d Representative blot of F4/80 (130 kDa) and α-tubulin (50 kDa) in sciatic nerve homogenates obtained from CX3CR1+/GFP and CX3CR1GFP/GFP mice at day 11. e Quantification of F4/80 band density normalised to α-tubulin (mean ± SEM, n = 3). RS-102985 significantly reduces VCR-associated infiltration into sciatic nerves obtained from CX3CR1GFP/GFP mice. NS not significant, *p < 0.05, one-way ANOVA, post hoc Tukey’s test

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