Distribution of malaria parasite-derived phosphatidylcholine in the infected erythrocyte
Distribution of malaria parasite-derived phosphatidylcholine in the infected erythrocyte
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感染红细胞中疟原虫来源的磷脂酰胆碱的分布
DOI：
10.1101/2023.03.13.532364
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发表时间：
2023
期刊：
影响因子：
--
通讯作者：
Vallintine T
中科院分区：
文献类型：
--
作者：
Vallintine T
疟疾寄生虫以多种方式修饰其宿主红细胞，导致宿主红细胞的变形性、渗透性和渗透性的变化。这些变化中的大多数是由从寄生虫输出到宿主红细胞的蛋白质介导的，在宿主红细胞中，这些蛋白质与宿主细胞的细胞骨架相互作用或在受感染的红细胞的质膜中形成复合物。此外，疟疾寄生虫诱导在感染的红细胞内形成膜隔室--寄生虫空泡、管泡网络（TVN）、毛雷尔裂和小泡--红细胞是一种正常情况下没有内膜的细胞。感染后，红细胞质膜的组成和不对称性也发生变化。虽然寄生虫蛋白质输出机制的许多方面已经变得清楚，但这些膜隔室形成和扩展的机制几乎完全未知。为了确定寄生虫衍生的磷脂是否在这些过程中发挥作用，我们应用了代谢标记技术，使磷脂酰胆碱被标记的荧光团。由于宿主红细胞不能合成磷脂，因此在感染的红细胞内，只有寄生虫来源的磷脂酰胆碱将用该技术标记。结果表明，由寄生虫产生的磷脂酰胆碱分布在整个感染的红细胞，包括TVN和红细胞质膜，但不是毛雷尔的裂缝。有趣的是，标记的磷脂也被检测到红细胞质膜入侵后不久的寄生虫，表明寄生虫可能会添加磷脂到宿主红细胞invasion.IMPORTANCEHere，我们描述了一个以前不受欢迎的方式，其中疟疾寄生虫与宿主红细胞相互作用，即，通过转移寄生虫磷脂到红细胞质膜。这可能对寄生虫在宿主细胞和宿主生物体中的存活具有重要影响。我们表明，寄生虫衍生的磷脂从寄生虫转移到宿主红细胞质膜和其他内膜后，寄生虫已侵入细胞产生的，至少部分地，使用寄生虫衍生的磷脂。唯一的例外是毛雷尔裂，这是一种膜状细胞器，参与将寄生虫蛋白质运输到红细胞表面。这表明毛雷尔裂是以不同于其他寄生虫诱导的膜的方式产生的。总的来说，这些发现提供了一个平台，研究一个新的方面的主机-寄生虫的相互作用。
Malaria parasites modify their host erythrocyte in multiple ways, leading to changes in the deformability, adhesiveness, and permeability of the host erythrocyte. Most of these changes are mediated by proteins exported from the parasite to the host erythrocyte, where these proteins interact with the host cell cytoskeleton or form complexes in the plasma membrane of the infected erythrocyte. In addition, malaria parasites induce the formation of membranous compartments—the parasitophorous vacuole, the tubovesicular network (TVN), the Maurer’s clefts and small vesicles—within the infected erythrocyte, a cell that is normally devoid of internal membranes. After infection, changes also occur in the composition and asymmetry of the erythrocyte plasma membrane. Although many aspects of the mechanism of export of parasite proteins have become clear, the mechanism by which these membranous compartments are formed and expanded is almost entirely unknown. To determine whether parasite-derived phospholipids play a part in these processes, we applied a metabolic labeling technique that allows phosphatidylcholine to be labeled with a fluorophore. As the host erythrocyte cannot synthesize phospholipids, within infected erythrocytes, only parasite-derived phosphatidylcholine will be labeled with this technique. The results revealed that phosphatidylcholine produced by the parasite is distributed throughout the infected erythrocyte, including the TVN and the erythrocyte plasma membrane, but not Maurer’s clefts. Interestingly, labeled phospholipids were also detected in the erythrocyte plasma membrane very soon after invasion of the parasites, indicating that the parasite may add phospholipids to the host erythrocyte during invasion.IMPORTANCEHere, we describe a previously unappreciated way in which the malaria parasite interacts with the host erythrocyte, namely, by the transfer of parasite phospholipids to the erythrocyte plasma membrane. This likely has important consequences for the survival of the parasite in the host cell and the host organism. We show that parasite-derived phospholipids are transferred from the parasite to the host erythrocyte plasma membrane and that other internal membranes that are produced after the parasite has invaded the cell are produced, at least in part, using parasite-derived phospholipids. The one exception to this is the Maurer’s cleft, a membranous organelle that is involved in the transport of parasite proteins to the surface of the erythrocyte. This reveals that the Maurer’s cleft is produced in a different manner than the other parasite-induced membranes. Overall, these findings provide a platform for the study of a new aspect of the host-parasite interaction.
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影响因子：
3.5
作者：
MOLL, GN;VIAL, HJ;VANDEENEN, LLM
通讯作者：
VANDEENEN, LLM
影响因子：
11.3
作者：
Sherling ES;van Ooij C
通讯作者：
van Ooij C
影响因子：
6.7
作者：
Fraser M;Jing W;Bröer S;Kurth F;Sander LE;Matuschewski K;Maier AG
通讯作者：
Maier AG
DOI：
10.1084/jem.149.1.172
发表时间：
1979-01-01
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Miller LH;Aikawa M;Johnson JG;Shiroishi T
通讯作者：
Shiroishi T
使用高度特异性激酶抑制剂快速、简单且精确地同步恶性疟原虫和诺氏疟原虫无性血期寄生虫
影响因子：
3.7
作者：
M. Ressurreição;James A. Thomas;S. Nofal;Christian Flueck;R. Moon;D. Baker;C. van Ooij
通讯作者：
C. van Ooij