Studies on the mechanism by which malaria parasites invade erythrocytes using host erythrocyte-derived ATP

结果表明：i）ATP在爆发时从感染的红细胞中释放。ii）ATP刺激导致dematin磷酸化，导致膜骨架松弛。iii）P2Y11受体拮抗剂抑制疟原虫侵入红细胞。iv）在ATP水解酶的存在下，寄生虫的侵入被抑制。总之，这强烈暗示恶性疟原虫侵入红细胞的过程需要宿主红细胞来源的ATP，然后ATP刺激P2Y11介导的信号通路，导致dematin磷酸化，并使红细胞膜骨架松弛。关闭上述信号通路的药物可能会提供一种保护人类免受疟疾侵害的新策略。

It was demonstrated that: i) ATP was released from infected erythrocytes upon burst. ii) ATP-stimulation resulted in phosphorylation of dematin, leading to loosening of membrane skeleton. iii) P2Y11 receptor antagonists inhibited malaria parasite invasion of erythrocytes. iv) The parasite invasion was inhibited in the presence of ATP-hydrolyzing enzymes. Altogether, it was strongly implicated that invasion process of erythrocytes by Plasmodium falciparum requires host erythrocyte-derived ATP, which then stimulates P2Y11-mediated signaling pathway, leading to phosphorylation of dematin, and loosening of erythroycte membrane skeleton. Drugs which shut down the above-mentioned signaling pathway might provide a novel strategy to protect humans from malaria.