Manuelidis L, Fritch W, Xi Y G
Section of Neuropathology, Yale Medical School, 310 Cedar Street, New Haven, CT 06510, USA.
Science. 1997 Jul 4;277(5322):94-8. doi: 10.1126/science.277.5322.94.
Bovine spongiform encephalopathy (BSE) has become a public health issue because a recently evolved BSE agent has infected people, yielding an unusual form of Creutzfeld-Jakob disease (CJD). A new CJD agent that provokes similar amyloid plaques and cerebellar pathology was serially propagated. First-passage rats showed obvious clinical signs and activated microglia but had negligible PrP-res (the more protease-resistant form of host PrP) or cerebellar lesions. Microglia and astrocytes may participate in strain selection because the agent evolved, stabilized, and reproducibly provoked BSE-like disease in subsequent passages. Early vacuolar change involving activated microglia and astrocytes preceded significant PrP-res accumulation by more than 50 days. These studies reveal several inflammatory host reactions to an exogenous agent.
牛海绵状脑病（BSE）已成为一个公共卫生问题，因为一种最近进化的BSE病原体感染了人类，导致了一种不寻常形式的克雅氏病（CJD）。一种能引发类似淀粉样斑块和小脑病变的新型CJD病原体被连续传代。第一代传代大鼠表现出明显的临床症状且小胶质细胞被激活，但PrP-res（宿主PrP更具蛋白酶抗性的形式）或小脑病变可忽略不计。小胶质细胞和星形胶质细胞可能参与毒株选择，因为该病原体在随后的传代中发生进化、稳定并可重复引发类似BSE的疾病。涉及激活的小胶质细胞和星形胶质细胞的早期空泡变化比显著的PrP-res积累早50多天出现。这些研究揭示了宿主对外源病原体的几种炎症反应。
