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Enhanced Egress of Intracellular Eimeria tenella Sporozoites by Splenic Lymphocytes from Coccidian-Infected Chickens

机译:球虫感染的鸡脾脏淋巴细胞对胞内艾美耳球虫孢子虫的出口增强作用

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Egress, which describes the mechanism that some intracellular parasites use to exit from parasitophorous vacuoles and host cells, plays a very important role in the parasite life cycle and is central to Eimeria propagation and pathogenesis. Despite the importance of egress in the intracellular parasite's life cycle, very little information is known on this process compared to other steps, e.g., invasion. The present study was conducted to investigate the interplay between the host adaptive immune system and Eimeria egression. Splenic lymphocytes or soluble immune factors were incubated with parasite-infected host cells for 3 or 5 h, and the percentage of egress was calculated according to an established formula. Viability of egressed parasites and host cells was tested using trypan blue exclusion and annexin V and propidium iodide staining, respectively. We found that premature egression of sporozoites from Eimeria tenella-infected primary chicken kidney cells or from chicken peripheral blood mononuclear cells occurred when the cells were cocultured in vitro with spleen lymphocytes from E. tenella-infected chickens but not when they were cocultured with splenocytes from uninfected chickens. Eimeria-specific antibodies and cytokines (gamma interferon [IFN-γ], interleukin-2 [IL-2], and IL-15), derived from E. tenella-primed B and T lymphocytes, respectively, were capable of promoting premature egress of sporozoites from infected host cells. Both egressed parasites and host cells were viable, although the latter showed reduced reinvasion ability. These results suggest a novel, immune-mediated mechanism that the host exploits to interrupt the normal Eimeria life cycle in vivo and thereby block the release of mature parasites into the environment.
机译:出口描述了一些细胞内寄生虫用于从寄生虫空泡和宿主细胞中逃逸的机制,在寄生虫的生命周期中起着非常重要的作用,对艾美球虫的繁殖和发病机制至关重要。尽管出口在细胞内寄生虫的生命周期中很重要,但与其他步骤(例如入侵)相比,该过程的信息知之甚少。进行本研究以研究宿主适应性免疫系统和艾美尔球虫出口之间的相互作用。将脾淋巴细胞或可溶性免疫因子与被寄生虫感染的宿主细胞孵育3或5 h,然后根据确定的公式计算出出百分比。分别使用台盼蓝排除法和膜联蛋白V和碘化丙锭染色测试了流出的寄生虫和宿主细胞的活力。我们发现,当将这些细胞与大肠杆菌感染的小鼠的脾淋巴细胞进行体外共培养时,孢子虫会从艾美球虫感染的艾美尔球虫感染的原代鸡肾细胞或鸡外周血单个核细胞中过早地逸出当它们与未感染鸡的脾细胞共培养时。分别来自于大肠杆菌(E. tenella)的B和T淋巴细胞衍生的艾美球虫特异性抗体和细胞因子(γ干扰素[IFN-γ],白介素2 [IL-2]和IL-15)能够促进早产。来自感染宿主细胞的子孢子。流出的寄生虫和宿主细胞都可行,尽管后者显示出降低的再侵袭能力。这些结果表明宿主可以利用一种新的,免疫介导的机制来中断体内正常的艾美叶虫生命周期,从而阻止成熟的寄生虫释放到环境中。

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