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首页> 外文期刊>Microbiology >In vivo programmed cell death of Entamoeba histolytica trophozoites in a hamster model of amoebic liver abscess
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In vivo programmed cell death of Entamoeba histolytica trophozoites in a hamster model of amoebic liver abscess

机译:在昆虫肝脓肿的仓鼠模型中的体内编程细胞死亡ontamoeba组织rootictica滋养体

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Entamoeba histolytica trophozoites can induce host cell apoptosis, which correlates with the virulence of the parasite. This phenomenon has been seen during the resolution of an inflammatory response and the survival of the parasites. Other studies have shown that E. histolytica trophozoites undergo programmed cell death (PCD) in vitro, but how this process occurs within the mammalian host cell remains unclear. Here, we studied the PCD of E. histolytica trophozoites as part of an in vivo event related to the inflammatory reaction and the host–parasite interaction. Morphological study of amoebic liver abscesses showed only a few E. histolytica trophozoites with peroxidase-positive nuclei identified by terminal deoxynucleotidyltransferase enzyme-mediated dUTP nick end labelling (TUNEL). To better understand PCD following the interaction between amoebae and inflammatory cells, we designed a novel in vivo model using a dialysis bag containing E. histolytica trophozoites, which was surgically placed inside the peritoneal cavity of a hamster and left to interact with the host’s exudate components. Amoebae collected from bags were then examined by TUNEL assay, fluorescence-activated cell sorting (FACS) and transmission electron microscopy. Nuclear condensation and DNA fragmentation of E. histolytica trophozoites were observed after exposure to peritoneal exudates, which were mainly composed of neutrophils and macrophages. Our results suggest that production of nitric oxide by inflammatory cells could be involved in PCD of trophozoites. In this modified in vivo system, PCD appears to play a prominent role in the host–parasite interaction and parasite cell death.
机译:entamoeba组织醇滋养滋生蛋白可以诱导宿主细胞凋亡,与寄生虫的毒力相关。在分辨炎症反应和寄生虫的存活期间已经看到这种现象。其他研究表明,E.组织组织滋养体在体外进行编程的细胞死亡(PCD),但是如何在哺乳动物宿主细胞内发生该过程仍然不清楚。在这里,我们研究了E.组织的PCD,作为与炎症反应和宿主寄生虫相互作用相关的体内事件的一部分。 Amoebic肝脏脓肿的形态学研究仅显示了末端脱氧核苷酸转移酶酶介导的DUTP缺口末端标记(TUNEL)鉴定的过氧化物酶阳性核的组织溶酶型滋养细胞。为了更好地理解PCD,在AmoEbae和炎性细胞之间的相互作用之后,我们使用含有E.组织晶体的透析袋设计了一种在体内模型中的新颖,其在仓鼠的腹腔内置于仓鼠的腹腔内,并与宿主的渗出物组分相互作用。然后通过TUNEL测定,荧光激活的细胞分选(FACS)和透射电子显微镜检查从袋子中收集的amoebae。在暴露于腹膜渗出物后观察到E.组织晶体滋养的核凝结和DNA片段化。主要由中性粒细胞和巨噬细胞组成。我们的研究结果表明,通过炎性细胞生产一氧化氮可参与滋养体的PCD。在这种在体内系统的改性中,PCD似乎在寄生虫相互作用和寄生虫细胞死亡中发挥着突出的作用。

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