Ho M, Singh B, Looareesuwan S, Davis T M, Bunnag D, White N J
Department of Clinical Tropical Medicine, Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand.
Infect Immun. 1991 Mar;59(3):873-8. doi: 10.1128/iai.59.3.873-878.1991.
To determine whether isolates of Plasmodium falciparum have intrinsically different cytoadherent properties and whether these differences contribute to the clinical severity of human falciparum malaria, we studied the cytoadherence to C32 melanoma cells in vitro of 59 parasite isolates from patients with naturally acquired infections in Thailand. Parasitized erythrocytes adhere to these melanoma cells principally via the glycoprotein CD36, which is also expressed on most vascular endothelium. In vitro cytoadherence was significantly greater for isolates from patients with biochemical evidence of severe malaria. The cytoadherent properties of P. falciparum parasites may thus be a virulence factor in human falciparum malaria. However, there was no correlation between the degree of in vitro cytoadherence and cerebral symptoms, which suggests that other receptors and/or host factors may be important in the adherence of malaria parasites to cerebral vascular endothelium. The cytokines tumor necrosis factor, interleukin-1, and gamma interferon, which have been implicated in the pathogenesis of cerebral malaria and are known to promote intercellular adhesion in other systems, did not enhance the cytoadherence of P. falciparum isolates to C32 melanoma cells.
为了确定恶性疟原虫分离株是否具有本质上不同的细胞黏附特性,以及这些差异是否导致人类恶性疟疾的临床严重程度,我们研究了来自泰国自然感染患者的59株寄生虫分离株在体外对C32黑色素瘤细胞的细胞黏附情况。被寄生的红细胞主要通过糖蛋白CD36黏附于这些黑色素瘤细胞,CD36也表达于大多数血管内皮细胞上。对于有严重疟疾生化证据患者的分离株,体外细胞黏附显著更强。因此,恶性疟原虫寄生虫的细胞黏附特性可能是人类恶性疟疾中的一种毒力因子。然而,体外细胞黏附程度与脑部症状之间并无关联,这表明其他受体和/或宿主因素在疟原虫黏附于脑血管内皮细胞过程中可能很重要。肿瘤坏死因子、白细胞介素-1和γ干扰素这些细胞因子与脑型疟疾的发病机制有关,并且已知在其他系统中可促进细胞间黏附,但它们并未增强恶性疟原虫分离株对C32黑色素瘤细胞的细胞黏附。