Fig. 5From: CXCL5 signaling is a shared pathway of neuroinflammation and blood–brain barrier injury contributing to white matter injury in the immature brainPharmacological inhibition of CXCR2 significantly attenuated microglial activation and BBB damage and protected against white matter injury after LPS-sensitized HI. A selective nonpeptide inhibitor of CXCR2, SB22 5002, was used to examine the role of the CXCL5–CXCR2 pathway in white matter injury after LPS-sensitized HI. After LPS + HI on P2, the SB-3 group (n = 9), but not the SB-1 group (n = 7), had significantly reduced ipsilateral ventricular size ratios (a), increased myelination (MBP) (b), and reduced astrogliosis (GFAP) (c) in the white matter on P12 compared with the vehicle-treated pups (n = 9). Scale bar = 100 μm. The SB-3 group (n = 9), but not the SB-1 group (n = 7), had a significantly reduced number of activated microglia (ED1) (d) and significantly lower BBB damage (IgG extravasation) (e) in the white matter compared with the vehicle group (n = 9) at 24 h after HI. Scale bar = 50 μm (ED1) and 100 μm (IgG); values are means ± SEMs, **p < 0.01Back to article page