Leukocyte-mediated mechanisms of brain damage after stroke

摘要

Ischemic stroke induces brain inflammation, involving chemokine-mediated leukocyte infiltration, which results in the progression of brain injury. Two of our recent studies investigated the role of specific leukocytes in outcome following stroke. In these studies, cerebral ischemia was induced in mice by middle cerebral artery occlusion for 0.5 h followed by reperfusion (ischemia-reperfusion; I-R). The first study provides evidence that T cells produce significantly more Nox2-dependent superoxide following I-R. The second study utilized a neutrophil CXCR2 antagonist that significantly reduced the infiltration of neutrophils, but had no effect on motor impairment or infarct volume at 72 h. Therefore, T cells may be a source of superoxide following I-R, but the brain infiltration of neutrophils may not contribute to stroke damage. Recent evidence suggests that some leukocytes may also contribute to brain regeneration following cerebral I-R, suggesting that much more research is required to elucidate which leukocytes contribute to post-ischemic injury.