临床儿科杂志
臨床兒科雜誌
림상인과잡지
2010年
8期
701-709
,共9页
汪咏梅%向伟%圣蒂·莫尔
汪詠梅%嚮偉%聖蒂·莫爾
왕영매%향위%골체·막이
CD73%弓形虫%鼠
CD73%弓形蟲%鼠
CD73%궁형충%서
CD73%Toxoplasma gondii%mice
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.
目的 探索CD73在弓形蟲感染中的作用及宿主細胞缺乏CD73時是否存在更少的弓形蟲感染和細胞內繁殖.方法 經口飼弓形蟲包囊,感染CD73缺乏和正常的小鼠.調查感染弓形蟲後.兩種小鼠的臨床癥狀、生存率、小腸病理學和細胞因子產生等.用帶熒光的弓形蟲子體感染CD73缺乏和正常的巨噬細胞和樹突狀細胞,調查兩種細胞的感染率、入侵到細胞內子體的數量及其在細胞內繁殖情況.結果 急性弓形蟲感染時,與CD73正常小鼠相比,CD73缺乏小鼠的生存率高,臨床癥狀輕,病理改變少.與CD73正常的巨噬細胞和樹突狀細胞相比,CD73缺乏的巨噬細胞和樹突狀細胞的弓形蟲感染率低,入侵到胞內的弓形蟲子體數目少,且繁殖速度慢.結論 CD73作為一種GPI細胞錶麵蛋白不僅可能參與瞭弓形蟲的液泡膜形成,而且可能有利于其侵犯宿主,以及弓形蟲子體在宿主細胞內的繁殖.缺乏CD73宿主可能牴抗弓形蟲感染的能力更彊.
목적 탐색CD73재궁형충감염중적작용급숙주세포결핍CD73시시부존재경소적궁형충감염화세포내번식.방법 경구사궁형충포낭,감염CD73결핍화정상적소서.조사감염궁형충후.량충소서적림상증상、생존솔、소장병이학화세포인자산생등.용대형광적궁형충자체감염CD73결핍화정상적거서세포화수돌상세포,조사량충세포적감염솔、입침도세포내자체적수량급기재세포내번식정황.결과 급성궁형충감염시,여CD73정상소서상비,CD73결핍소서적생존솔고,림상증상경,병리개변소.여CD73정상적거서세포화수돌상세포상비,CD73결핍적거서세포화수돌상세포적궁형충감염솔저,입침도포내적궁형충자체수목소,차번식속도만.결론 CD73작위일충GPI세포표면단백불부가능삼여료궁형충적액포막형성,이차가능유리우기침범숙주,이급궁형충자체재숙주세포내적번식.결핍CD73숙주가능저항궁형충감염적능력경강.
Objective To explore the role of CD73 in Toxoplasma gondii (T. Gondii) infection; To verify the host cells absent with CD73 would have less infection and replication of T. Gondii. Methods CD73 knockout and wild-type mice were infected with 20 cysts of ME 49 by oral gavage. The survival rate, clinic symptoms, pathology in the gut, and cytokine production were investigated in infected mice. Macrophages and dendritic cells with CD73-/- and CD73+/+ were infected with RH-YFP. The infective rates, the number of intracellular RH-YFP in the host cells, and the replication of intracellular RH-YFP were detected in these two type cells. Results CD73 knockout mice had a higher survival rate and milder clinic presentation with less morphologies in the gut in the acute T. Gondii infection compared with wild-type mice. CD73-/- macrophages and dentritic cells had less T. Gondii infection, and less intracellular parasite number and replication compared with CD73+/+ macrophages and dentritic cells in vitro. Conclusions CD73 as a GPI-anchored surface protein of host cell might be involved in forming the parasite vacuole, and promote the parasite's attachment and invasion of host eeUs. Host cells absence with CD73 would be less infection and replication of T. Gondii, and relative resistant parasites infection.
