【摘要】：目的探討Toll樣受體2(Toll-like receptors 2,TLR2)在伯氏瘧原蟲ANKA株(Plasmodium berghei ANKA,Pb ANKA)誘導(dǎo)的實驗?zāi)X型瘧(experimental cerebral malaria,ECM)中的作用。方法取Pb ANKA采用蚊叮感染、子孢子定量感染和紅內(nèi)期原蟲感染3種方式感染TLR2-/-C57BL/6小鼠,同時以WT C57BL/6小鼠為對照。蚊叮感染時,先以Pb ANKA瘧原蟲感染斯氏按蚊,然后斯氏按蚊通過叮咬實驗小鼠使其感染瘧原蟲。子孢子定量感染時,先以Pb ANKA瘧原蟲感染斯氏按蚊,然后通過解剖按蚊唾液腺獲得瘧原蟲子孢子,定量注射感染實驗小鼠。紅內(nèi)期原蟲感染時,先以Pb ANKA瘧原蟲感染W(wǎng)T C57BL/6小鼠獲取感染瘧原蟲紅細(xì)胞(parasitized?Red?Blood?Cell,pRBC),然后用pRBC定量感染實驗小鼠。通過觀測實驗小鼠紅細(xì)胞原蟲率、存活率及ECM發(fā)生率,判定TLR2是否參與ECM的發(fā)生。結(jié)果蚊叮感染時,TLR2-/-C57BL/6小鼠與WT C57BL/6小鼠原蟲率在ECM發(fā)生期間(6~9d)無顯著差別,表明TLR2缺失對Pb ANKA瘧原蟲在小鼠體內(nèi)的增殖無顯著影響。兩組小鼠在感染6d后均開始出現(xiàn)偏癱、昏迷等典型CM癥狀,9d內(nèi)全部發(fā)生ECM并死亡,ECM發(fā)生率均為100%,小鼠存活率均為0。子孢子定量感染時,兩組實驗小鼠紅細(xì)胞原蟲率無顯著差異;小鼠存活率TLR2-/-組為0,WT組為10%;ECM發(fā)生率TLR2-/-組為100%,WT組為90%,均無顯著差異。紅內(nèi)期原蟲感染時,兩組實驗小鼠紅細(xì)胞原蟲率無顯著差異,感染后8d全部發(fā)生ECM并死亡,ECM發(fā)生率均為100%,小鼠存活率均為0。結(jié)論 3種感染實驗中小鼠TLR2缺失均未影響ECM的進(jìn)程,表明ECM的發(fā)生不依賴于TLR2的參與。
[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.
【作者單位】： 第三軍醫(yī)大學(xué)基礎(chǔ)醫(yī)學(xué)部病原生物學(xué)教研室;
【基金】：國家自然科學(xué)基金項目(No.81301456) 重慶市自然科學(xué)基金項目(No.cstc2012jjA10048)
【分類號】：R531.3

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