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诺氏疟原虫感染后猴红细胞中的磷脂组织

Phospholipid organization in monkey erythrocytes upon Plasmodium knowlesi infection.

作者信息

Van der Schaft P H, Beaumelle B, Vial H, Roelofsen B, Op den Kamp J A, Van Deenen L L

出版信息

Biochim Biophys Acta. 1987 Jul 10;901(1):1-14. doi: 10.1016/0005-2736(87)90250-1.

DOI:10.1016/0005-2736(87)90250-1
PMID:3593720
Abstract

The phospholipid organization in monkey erythrocytes upon Plasmodium knowlesi infection has been studied. Parasitized and nonparasitized erythrocytes from malaria-infected blood were separated and pure erythrocyte membranes from parasitized cells were isolated using Affi-Gel beads. In this way, the phospholipid content and composition of the membrane of nonparasitized cells, the erythrocyte membrane of parasitized cells and the parasite could be determined. The phospholipid content and composition of the erythrocyte membranes of nonparasitized and parasitized cells and erythrocytes from chloroquine-treated monkeys cured from malaria, were the same as in normal erythrocytes. The phospholipid content of the parasite increased during its development, but its composition remained unchanged. Three independent techniques, i.e., treatment of intact cells with phospholipase A2 and sphingomyelinase C, fluorescamine labeling of aminophospholipids and a phosphatidylcholine-transfer protein-mediated exchange procedure have been applied to assess the disposition of phospholipids in: erythrocytes from healthy monkeys, nonparasitized and parasitized erythrocytes from monkeys infected with Plasmodium knowlesi, and erythrocytes from monkeys that had been cured from malaria by chloroquine treatment. The results obtained by these experiments do not show any abnormality in phospholipid asymmetry in the erythrocyte from malaria-infected (splenectomized) monkeys, neither in the nonparasitized cells, nor in the parasitized cells at any stage of parasite development. Nevertheless, a considerable degree of lipid bilayer destabilization in the membrane of the parasitized cells is apparent from the enhanced exchangeability of the PC from those cells, as well as from their increased permeability towards fluorescamine.

摘要

对感染诺氏疟原虫的猴红细胞中的磷脂组织进行了研究。从疟疾感染的血液中分离出被寄生和未被寄生的红细胞,并使用Affi-Gel珠分离出被寄生细胞的纯红细胞膜。通过这种方式,可以确定未被寄生细胞的膜、被寄生细胞的红细胞膜以及寄生虫的磷脂含量和组成。未被寄生和被寄生细胞的红细胞膜以及经氯喹治疗已治愈疟疾的猴的红细胞中的磷脂含量和组成与正常红细胞相同。寄生虫的磷脂含量在其发育过程中增加,但其组成保持不变。已应用三种独立技术,即使用磷脂酶A2和鞘磷脂酶C处理完整细胞、对氨基磷脂进行荧光胺标记以及磷脂酰胆碱转移蛋白介导的交换程序,来评估磷脂在以下细胞中的分布:健康猴的红细胞、感染诺氏疟原虫的猴的未被寄生和被寄生的红细胞,以及经氯喹治疗已治愈疟疾的猴的红细胞。这些实验获得的结果表明,在感染疟疾(脾切除)的猴的红细胞中,无论是未被寄生的细胞还是在寄生虫发育的任何阶段的被寄生细胞,磷脂不对称性均未显示出任何异常。然而,从这些细胞中磷脂酰胆碱(PC)交换能力的增强以及它们对荧光胺通透性的增加可以明显看出,被寄生细胞的膜中存在相当程度的脂质双层不稳定。

相似文献

1
Phospholipid organization in monkey erythrocytes upon Plasmodium knowlesi infection.诺氏疟原虫感染后猴红细胞中的磷脂组织
Biochim Biophys Acta. 1987 Jul 10;901(1):1-14. doi: 10.1016/0005-2736(87)90250-1.
2
Phospholipid uptake by Plasmodium knowlesi infected erythrocytes.诺氏疟原虫感染的红细胞对磷脂的摄取
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An intracellular simian malarial parasite (Plasmodium knowlesi) induces stage-dependent alterations in membrane phospholipid organization of its host erythrocyte.一种细胞内猿疟原虫(诺氏疟原虫)会诱导其宿主红细胞膜磷脂组织发生阶段依赖性改变。
Biochem J. 1987 Aug 15;246(1):103-8. doi: 10.1042/bj2460103.
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Plasmodium knowlesi induces alterations in phosphatidylcholine and phosphatidylethanolamine molecular species composition of parasitized monkey erythrocytes.诺氏疟原虫可诱导被寄生的猴红细胞的磷脂酰胆碱和磷脂酰乙醇胺分子种类组成发生改变。
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Phospholipid asymmetry in the plasma membrane of malaria infected erythrocytes.
Biochem Cell Biol. 1990 Feb;68(2):579-85. doi: 10.1139/o90-083.
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Possible basis for membrane changes in nonparasitized erythrocytes of malaria-infected animals.疟疾感染动物未寄生红细胞膜变化的可能基础。
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Modification of host cell membrane lipid composition by the intra-erythrocytic human malaria parasite Plasmodium falciparum.红细胞内人类疟原虫恶性疟原虫对宿主细胞膜脂质成分的修饰。
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Heat-induced alterations in monkey erythrocyte membrane phospholipid organization and skeletal protein structure and interactions.热诱导的猴红细胞膜磷脂组织、骨架蛋白结构及相互作用的改变
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Transbilayer phospholipid asymmetry in Plasmodium knowlesi-infected host cell membrane.诺氏疟原虫感染的宿主细胞膜中的跨膜磷脂不对称性。
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Alterations in erythrocyte membrane phospholipid organization due to the intracellular growth of the human malaria parasite, Plasmodium falciparum.由于人类疟原虫恶性疟原虫在细胞内生长导致的红细胞膜磷脂组织改变。
Parasitology. 1991 Apr;102 Pt 2:179-86. doi: 10.1017/s0031182000062466.

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