期刊
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
卷 29, 期 9, 页码 1503-1516出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/jcbfm.2009.71
关键词
blood-cerebrospinal fluid barrier; choroid plexus; CXC chemokines; neutrophils; traumatic brain injury
资金
- NIH [NS49479, R07057CS]
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS049479] Funding Source: NIH RePORTER
Traumatic brain injury (TBI) frequently results in neuroinflammation, which includes the invasion of neutrophils. After TBI, neutrophils infiltrate the choroid plexus (CP), a site of the blood-cerebrospinal fluid (CSF) barrier (BCSFB), and accumulate in the CSF space near the injury, from where these inflammatory cells may migrate to brain parenchyma. We have hypothesized that the CP functions as an entry point for neutrophils to invade the injured brain. Using the controlled cortical impact model of TBI in rats and an in vitro model of the BCSFB, we show that the CP produces CXC chemokines, such as cytokine-induced neutrophil chemoattractant (CINC)-1 or CXCL1, CINC-2 alpha or CXCL3, and CINC-3 or CXCL2. These chemokines are secreted both apically and basolaterally from the choroidal epithelium, a prerequisite for neutrophil migration across epithelial barriers. Consistent with these findings, we also provide electron microscopic evidence that neutrophils infiltrate the choroidal stroma and subsequently reach the intercellular space between choroidal epithelial cells. This is the first detailed analysis of the BCSFB function related to neutrophil trafficking. Our observations support the role of this barrier in posttraumatic neutrophil invasion. Journal of Cerebral Blood Flow & Metabolism (2009) 29, 1503-1516; doi:10.1038/jcbfm.2009.71; published online 27 May 2009
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据