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本文研究人重组肿瘤坏死因子(rHuTNF)在体内对感染疟原虫小鼠巨噬细胞释放活性氧(ROS)的影响及其与降低原虫率的关系。感染约氏疟原虫小鼠连续注射rHuTNF2500U,原虫率比未注射rHuTNF的感染小鼠低。但两组死亡时间无差别。正常小鼠连续注射rHuTNF及免疫小鼠再感染时,无一死亡。应用化学发光法检测,发现rHuTNF显著增强正常小鼠和感染小鼠腹腔渗出细胞(PEC)产生的ROS,甚至高于免疫小鼠PEC产生的ROS。小鼠感染疟原虫后,每天注射rHuTNF2500U,PEC产生ROS的高峰在感染后6d。感染过程中,rHrTNF促使PEC释放ROS与疟原虫生长抑制率无相关性。结果提示在疟疾感染时,rHuTNF增强巨噬细胞的氧化杀伤功能以及在体内抑制疟原虫生长。在复杂的疟疾免疫中,TNF可能作为免疫调节剂,与其他细胞因子协同起作用。
The aim of this study was to investigate the effect of rHuTNF on the release of reactive oxygen species (ROS) from macrophages infected with Plasmodium falciparum and its relationship with the reduction of protozoal in vivo. Infected P. yoelii mice were injected consecutively with rHuTNF 2500U, with a lower parasite rate than infected mice not injected with rHuTNF. However, there was no difference in death time between the two groups. When normal mice were injected with rHuTNF continuously and re-infected with immunized mice, none of them died. Using chemiluminescence detection, rHuTNF was found to significantly increase the ROS production in peritoneal exudate cells (PECs) of normal and infected mice even higher than that of PEC-immunized mice. After the mice were infected with Plasmodium, rHuTNF2500U was injected daily, and the peak of ROS production by PEC was 6 days after infection. In the course of infection, rHrTNF did not induce PEC to release ROS and had no correlation with growth inhibition rate of Plasmodium. The results suggest that rHuTNF enhances the macrophage oxidative killing function and inhibits the growth of malaria parasite in vivo during malaria infection. In complex malaria immunization, TNF may act as an immunomodulator and act synergistically with other cytokines.