A switch in infected erythrocyte deformability at the maturation and blood circulation of Plasmodium falciparum transmission stages
A switch in infected erythrocyte deformability at the maturation and blood circulation of Plasmodium falciparum transmission stages
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DOI：
10.1182/blood-2012-03-414557
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发表时间：
2012-06-14
期刊：
影响因子：
20.3
通讯作者：
Lavazec, Catherine
中科院分区：
文献类型：
--
作者：
Tiburcio, Marta;Niang, Makhtar;Lavazec, Catherine
实现消灭疟疾需要制定新的战略，干扰寄生虫的传播，包括针对寄生虫的性阶段（配子体）。恶性疟原虫配子体在人类宿主中的形成需要数天时间，在此期间未成熟配子体感染的红细胞（GIE）在宿主组织中隔离。只有成熟阶段的GIE在外周血中循环，可被按蚊媒介摄取。GIE在循环中的隔离和释放的潜在机制实际上是未知的。我们在这里表明，成熟的GIEs比不成熟的阶段，使用ektacytometry和microsphiltration方法更易变形，并且在从不成熟到成熟配子体的过渡中，细胞变形性的切换伴随着寄生虫衍生的STEVOR蛋白从受感染的红细胞膜的解离。我们推测，机械保留有助于隔离未成熟的GIE和成熟配子母细胞的恢复变形性与它们在血流中的释放和循环能力有关。这些过程中发挥了关键作用，恶性疟原虫配子体发育的主机和代表新的和非传统的目标，干扰寄生虫传播。（血。2012; 119（24）：e172-e180）
Achievement of malaria elimination requires development of novel strategies interfering with parasite transmission, including targeting the parasite sexual stages (gametocytes). The formation of Plasmodium falciparum gametocytes in the human host takes several days during which immature gametocyte-infected erythrocytes (GIEs) sequester in host tissues. Only mature stage GIEs circulate in the peripheral blood, available to uptake by the Anopheles vector. Mechanisms underlying GIE sequestration and release in circulation are virtually unknown. We show here that mature GIEs are more deformable than immature stages using ektacytometry and microsphiltration methods, and that a switch in cellular deformability in the transition from immature to mature gametocytes is accompanied by the deassociation of parasite-derived STEVOR proteins from the infected erythrocyte membrane. We hypothesize that mechanical retention contributes to sequestration of immature GIEs and that regained deformability of mature gametocytes is associated with their release in the bloodstream and ability to circulate. These processes are proposed to play a key role in P falciparum gametocyte development in the host and to represent novel and unconventional targets for interfering with parasite transmission. (Blood. 2012; 119(24):e172-e180)