Cowen N L, Clancy R L, Stace J, Cripps A W
Aust N Z J Med. 1986 Jun;16(3):360-4. doi: 10.1111/j.1445-5994.1986.tb01187.x.
Cerebral malaria is a major form of complicated malaria consequent upon cerebral damage associated with endothelial cell necrosis. We have used assays of Plasmodium falciparum growth inhibition in vitro to study serum inhibitory factors in patients with cerebral malaria. Serum from children with cerebral malaria inhibited parasite growth in a non-synchronised 72-hour assay to a greater extent than did sera from immune adults or asymptomatic children (p less than 0.001). The high level of non-specific inhibition of parasite growth was particularly evident when sera were tested against three P. falciparum isolates, and contrasted with the inhibitory effect of sera from non-malaria febrile controls. In this study, serum from patients with cerebral malaria was more inhibitory than serum from the other groups (p less than 0.001) and its between-isolate variation, when tested against a panel of P. falciparum isolates in growth assays, was significantly less than that of the other groups tested (p less than 0.005). These results are consistent with the hypothesis of toxin-induced endothelial cell damage, with the sequence of pathogenic events involving host-derived serum factors capable of damaging P. falciparum.
脑型疟疾是复杂疟疾的一种主要形式,是由与内皮细胞坏死相关的脑损伤所致。我们利用体外恶性疟原虫生长抑制试验来研究脑型疟疾患者的血清抑制因子。在一项非同步的72小时试验中,脑型疟疾患儿的血清对寄生虫生长的抑制程度比免疫成人或无症状儿童的血清更大(p<0.001)。当用血清检测三种恶性疟原虫分离株时,寄生虫生长的非特异性抑制水平很高,这与非疟疾发热对照血清的抑制作用形成对比。在本研究中,脑型疟疾患者的血清比其他组的血清更具抑制性(p<0.001),并且在生长试验中用一组恶性疟原虫分离株检测时,其分离株间的变异性明显小于其他检测组(p<0.005)。这些结果与毒素诱导内皮细胞损伤的假说一致,致病事件的顺序涉及能够损伤恶性疟原虫的宿主来源血清因子。