Evans-Osses Ingrid, Mojoli Andres, Monguió-Tortajada Marta, Marcilla Antonio, Aran Veronica, Amorim Maria, Inal Jameel, Borràs Francesc E, Ramirez Marcel I
Fundacao Oswaldo Cruz-Instituto Oswaldo Cruz, Av. Brasil 4365, Manguinhos, Rio de Janeiro, Brazil.
REMAR-IVECAT Group, Health Science Research Institute Germans Trias i Pujol, Can Ruti Campus, Badalona, Spain.
Eur J Cell Biol. 2017 Mar;96(2):131-142. doi: 10.1016/j.ejcb.2017.01.005. Epub 2017 Jan 22.
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.
肠道贾第虫是一种厌氧原生动物，也是贾第虫病的病原体，这种腹泻病在全球范围内存在且与贫困相关。肠道贾第虫具有简单的生命周期，在包囊和滋养体之间交替。包囊经口传播至胃部，并通过多因素过程在肠道内转化为滋养体。最近，已发现微泡（MVs）可从多种真核细胞中释放。我们观察到在肠道贾第虫的生命周期中有微泡释放，鉴定出了来自活跃滋养体以及正分化为包囊形式的滋养体的微泡。当前研究的目的是调查肠道贾第虫微泡在贾第虫病发病机制中的作用。对数期的微泡能够增加肠道贾第虫滋养体与Caco - 2细胞的附着。此外，肠道贾第虫的微泡可被人未成熟树突状细胞捕获，导致人树突状细胞的活化和异体刺激增加。脂筏参与微泡生物发生以及与Caco - 2细胞的附着。然而，对两种类型微泡的蛋白质组学分析显示在蛋白质水平上存在细微差异。了解源自滋养体的微泡的生物发生和内容物可能对该疾病的发病机制具有重要意义。
