Fig. 2From: CXCR2 is essential for cerebral endothelial activation and leukocyte recruitment during neuroinflammationChemokine levels and the effect of CXCR2 or CXCL1 deficiency on neutrophil recruitment to the brain parenchyma after i.c.v. LPS injection. Wild-type mice were i.c.v. injected with LPS. CXCL1 (A), CXCL2 (B), and CXCL5 (C) concentrations in the brains of WT (C57BL/6J) mice were determined via ELISA at various time points after i.c.v. LPS injection. WT mice i.c.v. injected with saline for 24 h served as negative controls. Infiltrating neutrophils in the cortex (D) and hippocampus (E) were quantified via esterase staining of the brain sections 4, 12, 24, or 48 h after i.c.v. LPS or saline injection. (F) The WT, CXCR2−/−, and CXCL1 mice were i.c.v. injected with LPS 24 h before the quantification of infiltrating neutrophils. Representative photomicrographs of brain sections stained for esterase positive neutrophils (arrows) from wild-type, (G–I) CXCR2−/− and CXCL1 mice. Scale bar: 100 μm; 10 μm (inset). CXCR2 and CXCL1 deficiency significantly reduced neutrophil recruitment in the cortex (G), hippocampus (H), and choroid plexus (I). The results are presented as the means ± SEM and represent a minimum of five mice per group. *P < 0.05; **P < 0.01Back to article page