CXCR2 and ischemic stroke: CXCR2-mediated infiltration of neutrophils into reperfused tissue has been demonstrated to be a primary mediator of tissue injury in numerous ischemia/reperfusion models, including ischemic stroke [4], and neuroprotection associated with CXCR2 receptor blockade has been presumed to occur largely indirectly through attenuation of leukocyte migration and activation.