Infection & Immunity, Faculty of Biomedical & Life Sciences, University of Glasgow, Glasgow, Scotland, UK.
Parasite Immunol. 2011 Nov;33(11):637-41. doi: 10.1111/j.1365-3024.2011.01329.x.
Cerebral malaria is a major pathological complication of Plasmodium falciparum infection in humans. Epidemiological observations have suggested that the clinical evolution of P. falciparum infections may be influenced by the concurrent presence of another Plasmodium species. Infection of susceptible mouse strains with P. berghei ANKA (PbA) provides an experimental model of cerebral malaria which has been extensively used to identify different components of the immune system involved in cerebral malaria. This model has also been employed to investigate the influence of experimental mixed-Plasmodium-species infections on the expression of cerebral malaria; PbA-induced cerebral malaria is completely inhibited by the simultaneous presence of P. yoelii yoelii 17 X clone 1.1 parasites, and accumulation of CD8(+) T cells in the brain vasculature is abolished. We investigated whether brain levels of CD8(+) -T-cell-chemoattractant chemokines CCL3, CCL4 and CCL5 are reduced in these protected coinfected mice compared with PbA-infected mice. Coinfected mice were found to exhibit significantly reduced levels of all three chemokines on day 6 post-infection. This finding may contribute to the abolition of the accumulation of CD8(+) T cells in the brain vasculature and the prevention of the development of cerebral malaria in coinfected mice.
脑型疟疾是恶性疟原虫感染人类的主要病理并发症。流行病学观察表明，疟原虫感染的临床演变可能受到另一种疟原虫的同时存在的影响。易感小鼠感染伯氏疟原虫 ANKA（PbA）提供了一种脑型疟疾的实验模型，该模型已被广泛用于鉴定参与脑型疟疾的不同免疫系统成分。该模型还被用于研究实验性混合疟原虫感染对脑型疟疾表达的影响；同时存在约氏疟原虫 17X 克隆 1.1 寄生虫可完全抑制 PbA 诱导的脑型疟疾，并且 CD8+T 细胞在脑血管中的积聚被消除。我们研究了与 PbA 感染的小鼠相比，在这些受保护的混合感染的小鼠中，脑内 CD8+T 细胞趋化因子 CCL3、CCL4 和 CCL5 的水平是否降低。感染后第 6 天，我们发现混合感染的小鼠这三种趋化因子的水平均显著降低。这一发现可能有助于消除 CD8+T 细胞在脑血管中的积聚，并防止混合感染的小鼠发生脑型疟疾。
