Manipulation of host hepatocytes by the malaria parasite for delivery into liver sinusoids
Manipulation of host hepatocytes by the malaria parasite for delivery into liver sinusoids
复制标题
DOI：
10.1126/science.1129720
复制
发表时间：
2006-09-01
期刊：
影响因子：
56.9
通讯作者：
Heussler, Volker T.
中科院分区：
文献类型：
--
作者：
Sturm, Angelika;Amino, Rogerio;Heussler, Volker T.
疟原虫的裂殖子阶段感染红细胞并引起疾病症状，最初在宿主肝细胞内形成。然而，肝裂殖子到达肝脏血管（血窦）并在侵入红细胞之前逃离宿主免疫系统的机制仍然未知。在这里，我们表明，寄生虫诱导的死亡和脱离其宿主肝细胞，随后由寄生虫填充的囊泡（裂殖体）到窦腔的萌芽。寄生虫同时抑制宿主质膜外叶上的磷脂酰丝氨酸的暴露，其充当吞噬细胞的“吃我”信号。因此，肝细胞来源的裂体似乎确保寄生虫迁移到血液中并保护其免受宿主免疫。
The merozoite stage of the malaria parasite that infects erythrocytes and causes the symptoms of the disease is initially formed inside host hepatocytes. However, the mechanism by which hepatic merozoites reach blood vessels (sinusoids) in the liver and escape the host immune system before invading erythrocytes remains unknown. Here, we show that parasites induce the death and the detachment of their host hepatocytes, followed by the budding of parasite-filled vesicles (merosomes) into the sinusoid lumen. Parasites simultaneously inhibit the exposure of phosphatidylserine on the outer leaflet of host plasma membranes, which act as "eat me'' signals to phagocytes. Thus, the hepatocyte-derived merosomes appear to ensure both the migration of parasites into the bloodstream and their protection from host immunity.