Hunter C A, Roberts C W, Murray M, Alexander J
Department of Veterinary Medicine, University of Glasgow, Bearsden.
Parasite Immunol. 1992 Jul;14(4):405-13. doi: 10.1111/j.1365-3024.1992.tb00015.x.
C57Bl/10 ScSn mice infected with Toxoplasma gondii developed a meningoencephalitis, characterized by areas of tissue destruction and cellular infiltration including foci of neutrophils. Large numbers of cyst stages were found throughout the brain but were not always associated with inflammation. The use of immunocytochemistry to detect glial fibrillary acidic protein, an astrocyte specific marker, showed a widespread astrocyte activation. This was particularly prominent in areas of intense inflammation but cysts were negative for glial fibrillary acidic protein, indicating that astrocytes were not host cells for the bradyzoites. The use of the polymerase chain reaction to assist in the amplification of total brain RNA allowed the characterization of the cytokines being produced locally within the brains of infected animals. beta-actin transcripts were detected in all of the uninfected and infected mice. In only one of the seven uninfected control mice were other transcripts found. Transcripts for tumour necrosis factor-alpha, interleukin-1 alpha and beta, interleukin-6, macrophage inflammatory protein-1 and interferon-gamma as well as the CD4 marker were detected in all of the infected mice. However, transcripts for IL-2 and IL-4 were not present. Several of the cytokines present are capable of initiating meningeal inflammation and may play a role in the immunopathogenesis of toxoplasmic encephalitis.
感染刚地弓形虫的C57Bl/10 ScSn小鼠发生了脑膜脑炎，其特征为组织破坏区域和细胞浸润，包括中性粒细胞聚集灶。在整个大脑中发现了大量的包囊期，但并不总是与炎症相关。使用免疫细胞化学检测胶质纤维酸性蛋白（一种星形胶质细胞特异性标志物）显示广泛的星形胶质细胞活化。这在炎症强烈的区域尤为突出，但包囊对胶质纤维酸性蛋白呈阴性，表明星形胶质细胞不是缓殖子的宿主细胞。使用聚合酶链反应辅助扩增全脑RNA可以对感染动物脑内局部产生的细胞因子进行表征。在所有未感染和感染的小鼠中均检测到β-肌动蛋白转录本。在七只未感染的对照小鼠中，只有一只发现了其他转录本。在所有感染小鼠中均检测到肿瘤坏死因子-α、白细胞介素-1α和β、白细胞介素-6、巨噬细胞炎性蛋白-1和干扰素-γ以及CD4标志物的转录本。然而，未检测到IL-2和IL-4的转录本。存在的几种细胞因子能够引发脑膜炎症，并可能在弓形虫性脑炎的免疫发病机制中起作用。
