Poltera A A, Hochmann A, Rudin W, Lambert P H
Clin Exp Immunol. 1980 Jun;40(3):496-507.
The successful induction of cerebral trypanosomiasis in ordinary laboratory mice using Trypanosoma brucei brucei is reported. Sequential studies demonstrated the presence of trypanosomes in the interstitium of the choroid plexus at the fourth week after infection which correlated with the appearance of anti-trypanosomal antibodies, a rise of IgM and IgG serum levels and a rise of Clq binding activity as well as a decrease of C3 levels. Electronmicroscopic studies showed that the parasites were flagellated and localized extracellularly mainly in the interstitium of the choroid plexus. Granular immunofluorescent deposits of Ig and C3 were most marked in the choroid plexus. Electron-dense deposits suggestive of immune complexes were seen in subendothelial, interstitial and subependymal areas of the choroid plexus. Since autoantibodies to the brain were found in the serum of some mice, the possible involvement of autoimmune manifestations in the pathogenesis of cerebral lesions has to be considered. The pattern of inflammatory foci at the eighth week after infection was very similar to that observed in cerebral African trypanosomiasis in man. After treatment with ethidium bromide, trypanosomes persisted in the tissues when circulating parasites could no longer be detected. These observations suggest a sequential involvement of brain structures during African trypanosomiasis. Trypanosomes may first migrate from the vascular compartment into the interstitium of the choroid plexus, possible favoured by increased vascular permeability. Circulating immune complexes and complement activation may be involved at this state. Trypanosomes localized in the choroid plexus may then trigger a local immunologically mediated inflammatory reaction favouring the migration of trypanosomes into the CSF and further invasion of other cerebral structures.
据报道，使用布氏布氏锥虫在普通实验室小鼠中成功诱导出脑锥虫病。连续研究表明，感染后第四周脉络丛间质中存在锥虫，这与抗锥虫抗体的出现、血清IgM和IgG水平升高、Clq结合活性升高以及C3水平降低相关。电子显微镜研究显示，寄生虫有鞭毛，主要位于脉络丛间质的细胞外。Ig和C3的颗粒状免疫荧光沉积物在脉络丛中最为明显。在脉络丛的内皮下、间质和室管膜下区域可见提示免疫复合物的电子致密沉积物。由于在一些小鼠血清中发现了针对大脑的自身抗体，因此必须考虑自身免疫表现可能参与脑损伤的发病机制。感染后第八周炎症灶的模式与人类脑非洲锥虫病中观察到的非常相似。用溴化乙锭治疗后，当循环中的寄生虫无法再检测到时，锥虫仍存在于组织中。这些观察结果表明，在非洲锥虫病期间脑结构会依次受到影响。锥虫可能首先从血管腔迁移到脉络丛间质，血管通透性增加可能有利于这种迁移。循环免疫复合物和补体激活可能在此阶段起作用。然后，位于脉络丛中的锥虫可能引发局部免疫介导的炎症反应，有利于锥虫迁移到脑脊液中并进一步侵入其他脑结构。
