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Fig. 6 | Journal of Neuroinflammation

Fig. 6

From: CXCL5 signaling is a shared pathway of neuroinflammation and blood–brain barrier injury contributing to white matter injury in the immature brain

Fig. 6

CXCL5-sensitized HI induced microglial activation, neutrophil infiltration, and BBB damage and caused white matter injury. Intracerebroventricular infusion of recombinant CXCL5 (1 or 2 μg) or NS followed by HI on P2 showed that the 2-μg CXCL5 + HI group (n = 6), but not the 1-μg CXCL5 + HI group (n = 6), had significantly higher ipsilateral ventricle size ratios (a), lower myelination (MBP) (b), and higher astrogliosis (GFAP) (c) in the white matter compared with the NS (n = 6) and the control groups (n = 6) on P12. Scale bar = 100 μm. At 24 h after HI, the 2-μg CXCL5 + HI (n = 6) and LPS + HI groups (n = 6) had a significantly higher number of activated microglia (ED1) (d) and BBB damage (e) in the white matter compared with the NS (n = 6) and control groups (n = 6). The 2-μg CXCL5 + HI group, but not the LPS + HI group, had significantly increased neutrophil infiltrations (MPO) (d) in the white matter. Scale bar = 50 μm (ED1) and 100 μm (IgG and MPO); values are means ± SEMs, **p < 0.01

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