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恶性疟原虫在人类红细胞中形成的寄生泡膜的起源。

Origins of the parasitophorous vacuole membrane of the malaria parasite, Plasmodium falciparum, in human red blood cells.

作者信息

Dluzewski A R, Mitchell G H, Fryer P R, Griffiths S, Wilson R J, Gratzer W B

机构信息

Medical Research Council Muscle and Cell Motility Unit, King's College, London, UK.

出版信息

J Cell Sci. 1992 Jul;102 ( Pt 3):527-32. doi: 10.1242/jcs.102.3.527.

Abstract

We have attempted to determine whether the parasitophorous vacuole membrane, in which the malaria parasite (merozoite) encapsulates itself when it enters a red blood cell, is derived from the host cell plasma membrane, as the appearance of the invasion process in the electron microscope has been taken to suggest, or from lipid material stored in the merozoite. We have incorporated into the red cell membrane a haptenic phospholipid, phosphatidylethanolamine, containing an NBD (N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)) group, substituted in the acyl chain, and allowed it to translocate into the inner bilayer leaflet. After invasion of these labelled cells by the parasite, Plasmodium falciparum, immuno-gold electron microscopy was used to follow the distribution of the labelled lipid; this was found to be overwhelmingly in favour of the host cell membrane relative to the parasitophorous vacuole. Merozoites of P. knowlesi were allowed to attach irreversibly to red cells without invasion, using the method of pretreatment with cytochalasin. The region of contact between the merozoite and the host cell membrane was in all cases devoid of the labelled phosphatidylethanolamine. These results lead us to infer that the parasitophorous vacuole membrane is derived wholly or partly from lipid preexisting in the merozoite.

摘要

我们试图确定疟原虫(裂殖子)进入红细胞时将自身包裹其中的寄生泡膜,是如电子显微镜下入侵过程的外观所暗示的那样源自宿主细胞质膜,还是源自裂殖子中储存的脂质物质。我们已将一种在酰基链中带有NBD(N -(7 - 硝基苯并 - 2 - 恶唑 - 1,3 - 二氮杂环丁烷 - 4 - 基))基团的半抗原磷脂——磷脂酰乙醇胺掺入红细胞膜中,并使其转移到内双层小叶中。在用恶性疟原虫对这些标记细胞进行侵袭后,使用免疫金电子显微镜来追踪标记脂质的分布;结果发现,相对于寄生泡而言,标记脂质绝大多数存在于宿主细胞膜中。利用细胞松弛素预处理的方法,使诺氏疟原虫裂殖子不可逆地附着于红细胞但不发生侵袭。在所有情况下,裂殖子与宿主细胞膜之间的接触区域均未发现标记的磷脂酰乙醇胺。这些结果使我们推断,寄生泡膜全部或部分源自裂殖子中预先存在的脂质。

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