Microglial cell loss after ischemic stroke favors brain neutrophil accumulation.

摘要: Stroke attracts neutrophils to the injured brain tissue where they can damage integrity of blood–brain barrier and exacerbate lesion. However, mechanisms involved in neutrophil transmigration, location accumulation ischemic are not fully elucidated. Neutrophils reach perivascular spaces vessels after crossing endothelial cell layer basal lamina post-capillary venules, or migrating from leptomeninges following pial vessel extravasation and/or a suggested translocation skull bone marrow. Based on previous observations microglia phagocytosing recruited lesion, we hypothesized that microglial cells might control brain. We studied a model permanent occlusion middle cerebral artery mice, including microglia- neutrophil-reporter mice. Using various vitro vivo strategies impair function eliminate by targeting colony stimulating factor 1 receptor (CSF1R), this study demonstrates phagocytosis has fundamental consequences for tissue. found reactive engulf at periphery whereas local loss dystrophy occurring core associated with first later parenchyma. Accordingly, depletion long-term treatment CSF1R inhibitor increased numbers enlarged Hence, phagocytic sets critical line defense against vascular damaging capacity ischemia.