Bone fracture exacerbates brain inflammation. Relative mRNA expression of interleukin (IL)-6 (A), IL-1β (B), and tumor necrosis factor (TNF)-α (C) 6h after bone fracture and 30h after the stroke in the stroke lesion (n = 5; [A] * P = 0.01 vs. stroke group without fracture, § P = 0.01 vs. bone fracture group; [B] # P < 0.001 vs. sham procedures for stroke § P < 0.001 vs. bone fracture group; [C] # P = 0.03 vs. the group subjected to sham procedures for stroke and § P = 0.002 vs. bone fracture group). The mice with stroke and bone fracture showed a trend toward higher IL-1β in the brain tissue than the mice with stroke only (P = 0.09). (D) Representative picture taken in the periinfarct region of CCR2^RFP/+CX3CR1^GFP/+ mice with stroke and bone fracture. D1. Low-magnified (scale bar: 100 μm) and D2, high-magnified (scale bar: 50 μm) images show that there are many CCR2⁺ (red) and CX3CR1⁺ (green) cells. Some cells are CCR2–CX3CR1 double positive (yellow). (E) The bar graph shows quantification of the percentage of CCR2⁺, CX3CR1⁺, or CCR2&CX3CR1⁺ cells amount total (4’,6-diamidino-2-phenylindole [DAPI]-positive nuclei) cells in the periinfarct region (n = 5, * P = 0.01 and ** P < 0.001).