Molecular Immunopathology Unit, The University of Sydney, Australia.
Int J Parasitol. 2011 Feb;41(2):155-63. doi: 10.1016/j.ijpara.2010.08.003. Epub 2010 Sep 7.
Cerebral malaria (CM) is a fatal complication of Plasmodium falciparum infection. Using a well defined murine model, we observed the effect on disease outcome of temporarily reducing parasite burden by anti-malarial drug treatment. The anti-malarial treatment regime chosen decreased parasitaemia but did not cure the mice, allowing recrudescence of parasites. These mice were protected against CM, despite their parasitaemia having increased, following treatment cessation, to levels surpassing that associated with CM in mice not treated with the drug. The protection was associated with reduced levels of cytokines, chemokines, CD8(+) T cells and parasites in the brain. The results suggest that the development of the immunopathological response that causes CM depends on a continuous stimulus provided by parasitised red blood cells, either circulating or sequestered in small vessels.
脑型疟疾（CM）是恶性疟原虫感染的一种致命并发症。我们使用一种明确的鼠模型，观察了通过抗疟药物治疗暂时降低寄生虫负担对疾病结局的影响。选择的抗疟治疗方案降低了寄生虫血症，但并未治愈小鼠，允许寄生虫重新出现。这些小鼠在停止治疗后，尽管其寄生虫血症增加到超过未用药物治疗的小鼠发生 CM 时的水平，但仍能免受 CM 的影响。保护作用与细胞因子、趋化因子、CD8(+)T 细胞和脑中寄生虫水平降低有关。结果表明，导致 CM 的免疫病理反应的发展取决于由寄生红细胞提供的持续刺激，这些红细胞要么循环，要么在小血管中被隔离。
