Chianella S, Semprevivo M, Peng Z C, Zaccheo D, Bentivoglio M, Grassi-Zucconi G
Department of Cell Biology, University of Perugia, Faculty of Biological Sciences, Via Elce di Sotto, Perugia, Italy.
Brain Res. 1999 Jun 19;832(1-2):54-62. doi: 10.1016/s0006-8993(99)01449-3.
Microglial cells play a key role in the events triggered by infection, injury or degeneration in the central nervous system not only as scavenger cells but also as immune effector elements. We analyzed the features and distribution of cells of the microglia/macrophage lineage with OX-42 and ED-1 immunohistochemistry in the brain of experimental rats infected with the extracellular parasite Trypanosoma brucei. Such experimental infection provides a rat model of sleeping sickness or African trypanosomiasis, and is hallmarked in its advanced stages by severe alterations of the animals' sleep structure. In infected rats a remarkable activation of microglia, revealed by OX-42 immunoreactivity, became evident in the 3rd week post-infection in periventricular and subpial brain regions, with a prevalence in the hypothalamus. These features were concomitant with the onset of sleep anomalies, monitored with electroencephalographic recordings. Microglia activation increased in the following weeks, paralleling the progressive alterations of sleep parameters, and was most marked in the terminal stages of the infection, corresponding to the 6th-7th weeks. In addition, ED-1-immunoreactive macrophages and ramified microglia, confined to hypothalamic periventricular and basal regions, were evident after 4 weeks of disease. Degeneration of neuronal perikarya was not detected histologically in the infected brains at any time point. These data provide evidence for a reaction of microglia and macrophages in the brain of trypanosome-infected rats, and point out a selective distribution of these activated cells. The findings are discussed in relation to the animals' sleep disorder during trypanosome infection.
小胶质细胞在中枢神经系统由感染、损伤或变性引发的事件中发挥关键作用，不仅作为吞噬细胞，还作为免疫效应元件。我们用OX - 42和ED - 1免疫组织化学分析了感染细胞外寄生虫布氏锥虫的实验大鼠脑中的小胶质细胞/巨噬细胞谱系细胞的特征和分布。这种实验性感染提供了昏睡病或非洲锥虫病的大鼠模型，其晚期特征是动物睡眠结构严重改变。在感染的大鼠中，OX - 42免疫反应性显示的小胶质细胞显著激活在感染后第3周在脑室周围和软脑膜下脑区变得明显，以下丘脑最为普遍。这些特征与通过脑电图记录监测到的睡眠异常的出现同时发生。在接下来的几周中小胶质细胞激活增加，与睡眠参数的逐渐改变平行，并且在感染的末期阶段最为明显，对应于第6 - 7周。此外，患病4周后，局限于下丘脑脑室周围和基底区域的ED - 1免疫反应性巨噬细胞和分支状小胶质细胞明显可见。在任何时间点，感染的大脑中均未通过组织学检测到神经元胞体的变性。这些数据为锥虫感染大鼠脑中的小胶质细胞和巨噬细胞反应提供了证据，并指出了这些活化细胞的选择性分布。结合锥虫感染期间动物的睡眠障碍对这些发现进行了讨论。
