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目的探索CD73在弓形虫感染中的作用及宿主细胞缺乏CD73时是否存在更少的弓形虫感染和细胞内繁殖。方法经口饲弓形虫包囊,感染CD73缺乏和正常的小鼠。调查感染弓形虫后,两种小鼠的临床症状、生存率、小肠病理学和细胞因子产生等。用带荧光的弓形虫子体感染CD73缺乏和正常的巨噬细胞和树突状细胞,调查两种细胞的感染率、入侵到细胞内子体的数量及其在细胞内繁殖情况。结果急性弓形虫感染时,与CD73正常小鼠相比,CD73缺乏小鼠的生存率高,临床症状轻,病理改变少。与CD73正常的巨噬细胞和树突状细胞相比,CD73缺乏的巨噬细胞和树突状细胞的弓形虫感染率低,入侵到胞内的弓形虫子体数目少,且繁殖速度慢。结论 CD73作为一种GPI细胞表面蛋白不仅可能参与了弓形虫的液泡膜形成,而且可能有利于其侵犯宿主,以及弓形虫子体在宿主细胞内的繁殖。缺乏CD73宿主可能抵抗弓形虫感染的能力更强。
Objective To explore the role of CD73 in Toxoplasma gondii infection and whether there is less Toxoplasma infection and intracellular reproduction in host cells lacking CD73. Methods Toxoplasma cysts were orally infected with CD73-deficient and normal mice. After investigation of Toxoplasma gondii infection, clinical symptoms, survival rates, pathologies of small intestine, and cytokine production in both mice were investigated. CD73-deficient and normal macrophages and dendritic cells were infected with fluorescent Toxoplasma gondii, the infection rates of both cells, the number of invaded intracellular and the intracellular multiplication were investigated. Results Acute Toxoplasma gondii infection, compared with CD73 normal mice, CD73-deficient mice with high survival rate, clinical symptoms, pathological changes less. CD73-deficient macrophages and dendritic cells have a low Toxoplasma infection rate compared with normal CD73-expressing macrophages and dendritic cells. The number of Toxoplasma gondii that invade into the cells is low and the rate of reproduction is slow. Conclusions As a GPI cell surface protein, CD73 may not only be involved in tonoplast formation of Toxoplasma gondii, but also may be beneficial to its invasion of host and the propagation of Toxoplasma gondii in host cells. Lack of CD73 host may be more resistant to Toxoplasma infection.