Institute of Laboratory Animals, Graduate School of Medicine, Kyorin University, Tokyo 181-8611, Japan.
Int J Parasitol. 2010 Jan;40(1):101-8. doi: 10.1016/j.ijpara.2009.08.009. Epub 2009 Sep 6.
Cerebral malaria is an infrequent but serious complication of Plasmodium falciparum infection in humans. Co-infection with different Plasmodium species is common in endemic areas and the existence of benign malaria parasites, such as Plasmodium vivax, during P. falciparum infection has been considered to reduce the risk of developing pathogenesis. However, it is still unknown how disease severity is reduced in the host during co-infection. In the present study, we investigated the influence of co-infection with non-lethal malaria parasites, Plasmodium berghei (Pb) XAT strain, on the outcome of Pb ANKA strain infection which causes experimental cerebral malaria (ECM) in mice. The co-infection with non-lethal Pb XAT suppressed ECM caused by Pb ANKA infection and prolonged survival of mice. The production of TNF-alpha and IFN-gamma, which had been shown to be involved in development of ECM, was suppressed in co-infected mice early in infection. The suppression of ECM by co-infection with Pb XAT was abrogated in IL-10-deficient mice. IL-10 plays a crucial role in the suppression of ECM by co-infection with non-lethal malaria parasites, probably due to its suppressive effect on the induction of TNF-alpha and IFN-gamma. Co-infection with Pb XAT and Pb ANKA is a useful model for understanding how ECM is suppressed.
脑型疟疾是人类感染恶性疟原虫后一种罕见但严重的并发症。在流行地区，同时感染不同疟原虫的情况很常见，并且在感染恶性疟原虫期间存在良性疟原虫，如间日疟原虫，被认为可以降低发病风险。然而，目前尚不清楚在宿主同时感染时，疾病的严重程度如何降低。在本研究中，我们研究了非致死性疟原虫感染，即感染伯氏疟原虫 XAT 株，对感染导致实验性脑型疟疾（ECM）的伯氏疟原虫 ANKA 株感染结果的影响。非致死性 Pb XAT 的共感染抑制了由 Pb ANKA 感染引起的 ECM，并延长了感染小鼠的存活时间。在感染早期，已显示与 ECM 发生有关的 TNF-α和 IFN-γ的产生在共感染小鼠中受到抑制。在 IL-10 缺陷型小鼠中，Pb XAT 共感染对 ECM 的抑制作用被消除。IL-10 在非致死性疟原虫共感染抑制 ECM 中起关键作用，可能是由于其对 TNF-α和 IFN-γ诱导的抑制作用。Pb XAT 和 Pb ANKA 的共感染是了解 ECM 如何被抑制的有用模型。
