S100BETA, AS A DETERMINANT FOR DEVELOPMENT OF MONOCYTE-DRIVEN ENCEPHALITIS

S100BETA，作为单核细胞驱动性脑炎发展的决定因素

• 批准号: 8172980
• 负责人: ANDREW G MACLEAN
• 金额: $ 6.18万
• 依托单位: TULANE UNIVERSITY OF LOUISIANA
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-05-01 至 2011-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8172980
• 关键词: Acquired Immunodeficiency Syndrome; Animals; Blood - brain barrier anatomy; Blood Vessels; Brain; Computer Retrieval of Information on Scientific Projects Database; Data; Deposition; Development; Encephalitis; Extravasation; Fibrinogen; Funding; Grant; Individual; Institution; Lesion; Macaca; Monitor; Neuropathogenesis; Pathogenesis; Plasma; Research; Research Personnel; Resources; SIV encephalitis; Serum; Source; Tight Junctions; United States National Institutes of Health; Urticaria; monocyte; neurotrophic protein S100beta; zonula occludens-1 protein

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The pathogenesis of HIV/SIV encephalitis (HIVE/SIVE) remains incompletely understood, but is associated with alterations in the blood brain barrier (BBB). Heretofore, it has not been possible to easily determine if an individual has HIVE/SIVE before post mortem examination. We have examined serum levels of the astroglial protein S100b in SIV-infected macaques and show that it can be used to predict which animals will develop SIVE. We also found that increased S100b protein in serum correlated with decreased expression of the tight junction protein zonula occludens-1 on brain microvessels. Further, the decrease in zonula occldens-1 expression was spatially related to SIVE lesions and perivascular deposition of plasma fibrinogen. Together these data indicate that SIVE lesions are associated with vascular leakage that can be monitored by S100b protein in the periphery. The ability to simply and prospectively monitor the development of SIVE will greatly facilitate studies of the neuropathogenesis of AIDS.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目及 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 HIV/SIV 脑炎 (HIVE/SIVE) 的发病机制尚不完全清楚，但与血脑屏障 (BBB) 的改变有关。迄今为止，在尸检之前还不可能轻易确定一个人是否患有 HIVE/SIVE。 我们检查了感染 SIV 的猕猴中星形胶质蛋白 S100b 的血清水平，结果表明它可以用来预测哪些动物会患上 SIVE。我们还发现，血清中 S100b 蛋白的增加与脑微血管上紧密连接蛋白 zonula occlusionns-1 表达的减少相关。 此外，zonula occldens-1 表达的减少在空间上与 SIVE 病变和血浆纤维蛋白原的血管周围沉积相关。这些数据共同表明，SIVE 病变与血管渗漏相关，可以通过外周的 S100b 蛋白进行监测。 简单、前瞻性地监测 SIVE 发展的能力将极大地促进艾滋病神经发病机制的研究。