Microvesicles released from Giardia intestinalis disturb host-pathogen response in vitro
Microvesicles released from Giardia intestinalis disturb host-pathogen response in vitro
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DOI：
10.1016/j.ejcb.2017.01.005
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发表时间：
2017-03-01
影响因子：
6.6
通讯作者：
Ramirez, Marcel I.
中科院分区：
文献类型：
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作者：
Evans-Osses, Ingrid;Mojoli, Andres;Ramirez, Marcel I.
贾第鞭毛虫（Giardia pigmentosa）是一种厌氧原生动物，也是贾第虫病的病原体，贾第虫病是一种世界性腹泻，与贫困有关。G.I有一个简单的生活周期，在包囊和滋养体之间交替。囊肿经口传播到胃，并通过多因素过程在肠内转化为滋养体。最近，微泡（MV）已被发现从广泛的真核细胞释放。我们已经观察到在G.I.的生命周期中MV的释放，从活动的滋养体和从分化成包囊形式的滋养体中鉴定MV。目前的工作的目的是调查的作用，从G.I的MV在贾第虫病的发病机制。对数生长期的MV能够增加G.此外，来自G. glucocorticoid的MV可以被人类未成熟树突状细胞捕获，导致人类树突状细胞的活化和同种异体刺激增加。脂筏参与MV的生物发生和与Caco-2细胞的附着。然而，两种类型的MV的蛋白质组学分析显示在蛋白质水平上略有差异。了解来源于滋养体的MV的生物起源和内容可能在疾病的发病机制中具有重要意义。(C)2017 Elsevier GmbH. All rights reserved.
Giardia intestinalis (G.I), is an anaerobic protozoan and the aetiological agent of giardiasis, a diarrhoea present worldwide and associated with poverty. G.I has a simple life cycle alternating between cyst and trophozoite. Cysts are transmitted orally to the stomach and transform to trophozoites in the intestine by a multifactorial process. Recently, microvesicles (MVs) have been found to be released from a wide range of eukaryotic cells. We have observed a release of MVs during the life cycle of G.I., identifying MVs from active trophozoites and from trophozoites differentiating to the cyst form. The aim of the current work was to investigate the role of MVs from G.I in the pathogenesis of giardiasis. MVs from log phase were able to increase the attachment of G.intestinalis trophozoites to Caco-2 cells. Moreover, MVs from G.intestinalis could be captured by human immature dendritic cells, resulting in increased activation and allostimulation of human dendritic cells. Lipid rafts participate in the MV biogenesis and in the attachment to Caco-2 cells. Nevertheless, proteomic analysis from two types of MVs has shown slight differences at the protein levels. An understanding of biogenesis and content of MVs derived from trophozoites might have important implications in the pathogenesis of the disease. (C) 2017 Elsevier GmbH. All rights reserved.