Curfs J H, van der Meer J W, Sauerwein R W, Eling W M
Department of Medical Microbiology, Faculty of Medicine, Catholic University of Nijmegen, The Netherlands.
J Exp Med. 1990 Nov 1;172(5):1287-91. doi: 10.1084/jem.172.5.1287.
In cerebral malaria, pathological changes can be found in the brain of infected people and in the brain of Plasmodium berghei-infected mice. The pathogenesis of cerebral malaria in mice is believed to be due to an immunopathological reaction giving rise to an excessive production of cytokines such as interferon gamma (IFN-gamma) and tumor necrosis factor (TNF). We find that low doses of interleukin 1 (IL-1) protect mice against cerebral malaria; IL-1 also inhibits parasitemia. The IL-1 effect on parasitemia was not observed in nude mice and was at least partly reversed in mice treated with IL-1 in combination with antibody to IFN-gamma, indicating the involvement of T cells. Mice protected against development of cerebral malaria by IL-1 treatment developed the syndrome when TNF was given as observed in control infected mice or infected mice treated with inactivated IL-1.
在脑型疟疾中,可在感染人群的大脑以及感染伯氏疟原虫的小鼠大脑中发现病理变化。小鼠脑型疟疾的发病机制被认为是由于免疫病理反应导致细胞因子如干扰素γ(IFN-γ)和肿瘤坏死因子(TNF)过度产生。我们发现低剂量的白细胞介素1(IL-1)可保护小鼠免受脑型疟疾的侵害;IL-1还能抑制寄生虫血症。在裸鼠中未观察到IL-1对寄生虫血症的影响,并且在用IL-1与抗IFN-γ抗体联合治疗的小鼠中,该影响至少部分被逆转,这表明T细胞参与其中。经IL-1治疗而免受脑型疟疾发展影响的小鼠,在给予TNF时会出现该综合征,这与对照感染小鼠或用灭活IL-1治疗的感染小鼠中观察到的情况相同。