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被恶性疟原虫感染的红细胞激活人类血小板。

[Erythrocytes infected by Plasmodium falciparum activate human platelets].

作者信息

Polack B, Peyron F, Sheick Zadiuddin I, Kolodié L, Ambroise-Thomas P

机构信息

Laboratoire d'Hématologie, C.N.R.S.-U.R.A. n. 1344, Faculté de Médecine de Grenoble, La Tronche.

出版信息

C R Acad Sci III. 1990;310(12):577-82.

PMID:2142012
Abstract

Blood platelets are involved in Plasmodium falciparum malaria pathology as shown by thrombocytopenia and increased plasma level of two alpha granule proteins: beta thromboglobulin (beta TG) and platelet factor 4 (PF4). In this study we demonstrate that Plasmodium falciparum parasitized erythrocytes activate directly the secretion of beta TG and PF4 by human platelets. This secretion is related to parasitemia and occurs immediately after contact. Treatment of parasited erythrocytes by trypsin and diffusion chamber experiments suggest that platelet activation is triggered by parasitic substances shed on erythrocyte membrane and released in the culture medium.

摘要

血小板减少以及两种α颗粒蛋白——β血小板球蛋白(βTG)和血小板第4因子(PF4)的血浆水平升高表明,血小板参与了恶性疟原虫疟疾的病理过程。在本研究中,我们证明,恶性疟原虫寄生的红细胞可直接激活人血小板分泌βTG和PF4。这种分泌与寄生虫血症有关,且在接触后立即发生。用胰蛋白酶处理寄生红细胞以及扩散小室实验表明,血小板激活是由红细胞膜上脱落并释放到培养基中的寄生物质触发的。

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