Sturm Angelika, Amino Rogerio, van de Sand Claudia, Regen Tommy, Retzlaff Silke, Rennenberg Annika, Krueger Andreas, Pollok Jörg-Matthias, Menard Robert, Heussler Volker T
Bernhard Nocht Institute for Tropical Medicine, Bernhard-Nocht-Strasse 74, 20359 Hamburg, Germany.
Science. 2006 Sep 1;313(5791):1287-90. doi: 10.1126/science.1129720. Epub 2006 Aug 3.
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.
感染红细胞并引发疾病症状的疟原虫裂殖子阶段最初在宿主肝细胞内形成。然而，肝内裂殖子到达肝脏血管（血窦）并在侵入红细胞之前逃避宿主免疫系统的机制仍不清楚。在此，我们表明寄生虫诱导其宿主肝细胞死亡和脱离，随后充满寄生虫的囊泡（裂殖子体）芽生进入血窦腔。寄生虫同时抑制宿主质膜外小叶上磷脂酰丝氨酸的暴露，而磷脂酰丝氨酸作为向吞噬细胞发出的“吃我”信号。因此，源自肝细胞的裂殖子体似乎既能确保寄生虫迁移到血液中，又能保护它们免受宿主免疫的影响。
