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Fig. 6 | Journal of Neuroinflammation

Fig. 6

From: High-salt diet decreases mechanical thresholds in mice that is mediated by a CCR2-dependent mechanism

Fig. 6

A CCR2 antagonist completely reversed the effects of an HSD on myeloid cell activation and mechanical hypersensitivity. a A CCR2 antagonist (RS 102895) was administered intraperitoneally for two consecutive days to mice after 3 months of HSD feeding. An anti-CCR2 (I.P.) treatment reduced the number of CD11b+CD115+ monocytes in the circulation to a normal level. b The anti-CCR2 (i.p.) treatment abolished the CCR2+Ly6Chi subset in the blood. c The CCR2 antagonist reduced the number of CD45+CD11b+F4/80+ macrophages, as well as the number of CD86+ macrophages, in the peripheral nerve to a level comparable to the macrophages of ND-fed mice, n = 6–8/group. d The expression of IL-1β and IL-6 in the peripheral nerves was significantly reduced by I.P. anti-CCR2 treatment, while the expression of IL-10 and CCL2 was not affected, n = 6/group. e, f Both the intraperitoneal (I.P.) and intrathecal (I.T.) administrations of the CCR2 antagonist inhibited HSD-induced spinal microglia activation, n = 6/group. Scale bar: 50 μm. The outline indicates the area of interest (lamina I–III) where microglia number was quantified. g, h Two days of treatment with either the I.P. or I.T. administration of the CCR2 antagonist successfully rescued the HSD-induced decreased mechanical thresholds to a normal level, n = 9–11/group. Data with ND-fed mice was included (green dotted line) as reference. No significant difference was observed between male and female mice; therefore, the data was combined. All data was presented as mean ± SEM and analyzed with an unpaired t test for ad and f or a two-way ANOVA followed by Bonferroni post-tests for g and f. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001

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