Department of Emergency Medicine, Alpert Medical School of Brown University, Providence, Rhode Island 02903, USA.
J Cereb Blood Flow Metab. 2012 Jan;32(1):93-104. doi: 10.1038/jcbfm.2011.111. Epub 2011 Aug 10.
The invasion of inflammatory cells occurring after ischemic or traumatic brain injury (TBI) has a detrimental effect on neuronal survival and functional recovery after injury. We have recently demonstrated that not only the blood-brain barrier, but also the blood-cerebrospinal fluid (CSF) barrier (BCSFB), has a role in posttraumatic recruitment of neutrophils. Here, we show that TBI results in a rapid increase in synthesis and release into the CSF of a major chemoattractant for monocytes, CCL2, by the choroid plexus epithelium, a site of the BCSFB. Using an in vitro model of the BCSFB, we also show that CCL2 is released across the apical and basolateral membranes of the choroidal epithelium, a pattern of chemokine secretion that promotes leukocyte migration across epithelial barriers. Immunohistochemical and electron microscopic analyses of choroidal tissue provide evidence for the movement of monocytes, sometimes in tandem with neutrophils, along the paracellular pathways between adjacent epithelial cells. These data further support the pathophysiological role of BCSFB in promoting the recruitment of inflammatory cells to the injured brain.
在缺血性或创伤性脑损伤（TBI）后发生的炎症细胞浸润对损伤后神经元的存活和功能恢复有不利影响。我们最近的研究表明，不仅血脑屏障，而且血脑脊液（CSF）屏障（BCSFB）在创伤后中性粒细胞的募集中起作用。在这里，我们表明 TBI 导致脉络丛上皮细胞迅速增加合成和释放到 CSF 中的单核细胞趋化因子 CCL2，脉络丛上皮细胞是 BCSFB 的一个部位。我们还使用 BCSFB 的体外模型表明，CCL2 是通过脉络丛上皮细胞的顶膜和基底外侧膜释放的，这种趋化因子分泌的模式促进白细胞穿过上皮屏障的迁移。脉络丛组织的免疫组织化学和电子显微镜分析为单核细胞（有时与中性粒细胞一起）沿相邻上皮细胞之间的细胞旁途径迁移提供了证据。这些数据进一步支持 BCSFB 在促进炎症细胞募集到受损大脑中的病理生理作用。
