弓形虫RH株ROP16I/III基因缺陷虫株感染BALB/c鼠的致病性研究

目的 旨在深入研究弓形虫棒状体效应分子ROP16与虫株毒力及致病性的关系。方法 采用弓形虫ROP16_I/III基因敲除RH株(RH_ΔROP16)攻击感染BALB/c小鼠,在感染后不同时间点与野生株感染鼠比较,动态观察感染动物发病症状、存活时间; HE染色观察脑组织、肺组织病理学差异,qRT-PCR检测脾细胞炎性及抑炎细胞因子表达水平。结果 两组小鼠的发病症状无明显差异;经HE染色显微镜下观察小鼠肺部及脑部病理学改变亦未见无明显差异;qRT-PCR检测并用Graph pad分析两组虫株感染小鼠的脾细胞Arg-1、IL-10、IL-12、TNF -α及IFN-γ等细胞因子表达水平。数据表明在感染相同时间ROP16缺陷株感染小鼠Arg-1的表达量明显低于野生型虫株(P< 0.05);而IL-10、IL-12、TNF-α和IFN -γ的表达水平无统计学差异(P> 0.05)。结论 I型弓形虫RH株的ROP16_I/III并非是决定急性感染期弓形虫毒力的唯一效应分子;ROP16_I/III可诱导宿主Arg-1高表达,提示与巨噬细胞内虫体的增殖有关。

Pathogenicity in BALB/c mice infection with Toxoplasma strain deficient in ROP16I/III

This study aims to explore the virulence and pathogenicity of ROP16, a rhoptry effector molecule of T. gondii. BALB/c mice were infected with wild type and ROP16_I/III gene knockout RH strain of T. gondii. Clinical signs and survival time were observed and histopathology of brain and lung tissues were examined by HE staining. Cytokines of splenocyte in infected animals were detected by qRT-PCR. No significant difference was observed in the pathogenicity between the two groups. HE staining showed no remarkable pathology difference in lung and brain tissues between the two groups of mice. Additionally, deletion of the effector ROP16_I/III did not impact expressed level of IL-10, IL-12, TNF-α and IFN-γ mRNA(P>0.05)except for the elevated level of Arg-1 mRNA (P<0.05). ROP16_I/III of type I strain of T.gondii may not be only, if any, the virulence-associated molecule during acute infection. ROP16_I/III enhance the Arg-1 expression, which is involved of the early proliferation in host cells.