Mechanisms underlying parasite induced permeability changes of the human erythrocyte membrane - how much is host, how much is parasite?

哺乳动物红细胞的寄生虫在缺乏营养的宿主细胞中生存，在那里它们被隔离在一个被称为寄生虫液泡的隔间里。它们通过在红细胞膜上诱导新的渗透途径从细胞外环境中获得必要的溶质，而这些途径在未感染的细胞中要么不存在，要么是沉默的。我们将使用恶性疟原虫(一种人类疟疾寄生虫)和巴贝斯虫(在人类中是一种机会性寄生虫)作为模式生物来描述这些途径形成的机制。总而言之，我们希望了解这些寄生虫在多大程度上利用其宿主细胞的特性，以及它们在多大程度上直接修改宿主细胞以增加其渗透性。具体地说，我们希望(I)揭开疟原虫感染激活沉默的红细胞谷氨酸转运体的机制，以及(Ii)确定疟原虫和巴贝斯虫在获取营养方面的异同。

Parasites of mammalian erythrocytes survive in a nutritionally deprived host cell, where they are secluded within a compartment termed the parasitophorous vacuole. They acquire essential solutes from the extracellular milieu by inducing new permeation pathways in the erythrocyte plasma membrane which are either not present or silent in the non-infected cell. We will use Plasmodium falciparum (a human malaria parasite) and Babesia divergens (in humans an opportunistic parasite) as model organisms to characterize the mechanisms involved in the formation of these pathways. In general terms, we wish to understand to what extent these parasites utilise properties of their host cell and to what extent they directly modify the host cell to increase its permeability. Specifically, we want (i) to unravel the mechanisms whereby infections with Plasmodium activate a silent erythrocyte glutamate transporter and (ii) define similarities and differences in nutrient acquisition by Plasmodium and Babesia.