Handayani Sarwo, Chiu Daniel T, Tjitra Emiliana, Kuo Jason S, Lampah Daniel, Kenangalem Enny, Renia Laurent, Snounou Georges, Price Ric N, Anstey Nicholas M, Russell Bruce
National Institute of Health Research and Development, Ministry of Health, Jakarta, Indonesia.
J Infect Dis. 2009 Feb 1;199(3):445-50. doi: 10.1086/596048.
Maturation of Plasmodium falciparum decreases the deformability of infected red blood cells (RBCs), increasing their clearance as they attempt to pass through endothelial slits of the splenic sinus. Previous studies of Plasmodium vivax-infected RBCs led to opposite conclusions with respect to cellular deformability. To resolve this controversy, P. vivax-infected RBCs were passed through a 2-microm microfluidic channel. In contrast to P. falciparum-infected RBCs, mature P. vivax-infected RBCs readily became deformed through 2-microm constrictions. After this extreme deformation, 67% of P. vivax-infected RBCs recovered a normal appearance; however, 15% of uninfected RBCs were destroyed. Results suggest mechanisms for both avoidance of splenic clearance and anemia in vivax malaria.
恶性疟原虫的成熟会降低被感染红细胞(RBCs)的可变形性,当它们试图穿过脾窦的内皮缝隙时,其清除率会增加。先前对间日疟原虫感染的红细胞的研究得出了关于细胞可变形性的相反结论。为了解决这一争议,将间日疟原虫感染的红细胞通过一个2微米的微流控通道。与恶性疟原虫感染的红细胞不同,成熟的间日疟原虫感染的红细胞很容易通过2微米的狭窄处而变形。经过这种极端变形后,67%的间日疟原虫感染的红细胞恢复了正常外观;然而,15%的未感染红细胞被破坏。结果提示了间日疟中避免脾脏清除和贫血的机制。