TLR2在实验脑型疟中的作用研究

发布时间：2019-06-17 08:21

【摘要】：目的探讨Toll样受体2(Toll-like receptors 2,TLR2)在伯氏疟原虫ANKA株(Plasmodium berghei ANKA,Pb ANKA)诱导的实验脑型疟(experimental cerebral malaria,ECM)中的作用。方法取Pb ANKA采用蚊叮感染、子孢子定量感染和红内期原虫感染3种方式感染TLR2-/-C57BL/6小鼠,同时以WT C57BL/6小鼠为对照。蚊叮感染时,先以Pb ANKA疟原虫感染斯氏按蚊,然后斯氏按蚊通过叮咬实验小鼠使其感染疟原虫。子孢子定量感染时,先以Pb ANKA疟原虫感染斯氏按蚊,然后通过解剖按蚊唾液腺获得疟原虫子孢子,定量注射感染实验小鼠。红内期原虫感染时,先以Pb ANKA疟原虫感染WT C57BL/6小鼠获取感染疟原虫红细胞(parasitized?Red?Blood?Cell,pRBC),然后用pRBC定量感染实验小鼠。通过观测实验小鼠红细胞原虫率、存活率及ECM发生率,判定TLR2是否参与ECM的发生。结果蚊叮感染时,TLR2-/-C57BL/6小鼠与WT C57BL/6小鼠原虫率在ECM发生期间(6~9d)无显著差别,表明TLR2缺失对Pb ANKA疟原虫在小鼠体内的增殖无显著影响。两组小鼠在感染6d后均开始出现偏瘫、昏迷等典型CM症状,9d内全部发生ECM并死亡,ECM发生率均为100%,小鼠存活率均为0。子孢子定量感染时,两组实验小鼠红细胞原虫率无显著差异;小鼠存活率TLR2-/-组为0,WT组为10%;ECM发生率TLR2-/-组为100%,WT组为90%,均无显著差异。红内期原虫感染时,两组实验小鼠红细胞原虫率无显著差异,感染后8d全部发生ECM并死亡,ECM发生率均为100%,小鼠存活率均为0。结论 3种感染实验中小鼠TLR2缺失均未影响ECM的进程,表明ECM的发生不依赖于TLR2的参与。
[Abstract]:Objective to investigate the role of Toll-like receptor 2 (Toll-like receptors 2, TLR2) in experimental cerebral malaria (experimental cerebral malaria,ECM induced by Plasmodium berghei ANKA strain (Plasmodium berghei ANKA,Pb ANKA. Methods TLR2-/-C57BL/6 mice were infected with Pb ANKA in three ways: mosquito bite infection, megaspore quantitative infection and intrared protozoa infection, and WT C57BL/6 mice were used as control. When mosquito bites, Anopheles stephensi is first infected with Plasmodium Pb ANKA, and then Anopheles stephensi is infected with Anopheles stephensi by biting experimental mice. When the spores were quantitatively infected, Anopheles stephensi was first infected with Plasmodium Pb ANKA, then the spores of Anopheles stephensi were obtained by dissecting the saliva gland of Anopheles, and the experimental mice were infected by quantitative injection. When WT C57BL/6 mice were infected with Plasmodium Pb ANKA, the red blood cells (parasitized?Red?Blood?Cell,pRBC) of Plasmodium falciparum were obtained, and then the mice were quantitatively infected with pRBC. The erythrocyte protozoa rate, survival rate and ECM incidence of experimental mice were observed to determine whether TLR2 was involved in the occurrence of ECM. Results there was no significant difference in protozoa rate between TLR2-/-C57BL/6 mice and WT C57BL/6 mice during ECM infection (6 脳 9 days), indicating that TLR2 deletion had no significant effect on the proliferation of Pb ANKA Plasmodium in mice. The typical CM symptoms such as paralysis and coma began to occur in both groups after 6 days of infection. ECM and death occurred in all mice within 9 days, the incidence of ECM was 100%, and the survival rate of mice was 0. 5%. There was no significant difference in erythrocyte protozoa rate between the two groups, the survival rate of mice was 0 in TLR2-/- group, 100% in WT group and 90% in WT group. There was no significant difference in erythrocyte protozoa rate between the two groups. ECM occurred and died 8 days after infection, the incidence of ECM was 100%, and the survival rate of mice was 0. 5%. Conclusion the deletion of TLR2 in three kinds of infection mice has no effect on the process of ECM, which indicates that the occurrence of ECM does not depend on the participation of TLR2.
【作者单位】：第三军医大学基础医学部病原生物学教研室;
【基金】：国家自然科学基金项目(No.81301456) 重庆市自然科学基金项目(No.cstc2012jjA10048)
【分类号】：R531.3

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