不同维生素免疫调节作用在鼠疟模型中的实验观察

探讨不同维生素对P. y17XL感染BALB/c小鼠的免疫调节作用。将6~8周龄,雌性BALB/c小鼠,随机分为维生素（ V）处理组和对照组。 V处理组小鼠分别经50 mg/kg VA、600 mg/kg VE 或1 g/只VC连续10 d灌胃,0.2 mL/只；对照组小鼠分别给予相同剂量的溶剂（大豆油或生理盐水）处理。之后,各组小鼠分别经腹腔接种1＆#215;106 P. y17XL寄生的红细胞,动态观察感染小鼠原虫血症水平和生存率；流式细胞术检测感染后第0、3和5天小鼠脾细胞树突状细胞（ DCs）亚群（ pDCs与mDCs）百分比及功能分子（ TLR9和MHC域）的表达。与对照组相比,VA和VE处理组小鼠原虫血症水平升高,生存率降低；感染后第5天脾细胞中pDCs与mDCs亚群水平以及DCs表面受体TLR9和表面分子MHC域的表达水平显著下降。相反,VC处理组小鼠原虫血症水平降低,生存率延长,pDCs与mDCs亚群以及TLR9和MHC域的表达水平显著升高。结果表明,不同维生素对疟疾感染产生不同的调控作用,VA和VE通过抑制DCs数量和功能,加重疟疾感染,而VC则促进DCs数量和功能,推迟感染进程。

Immuno-Regulatory Effects of Different Vitamins on Mouse Malaria Model

Immuno-regulation of different vitamins on BALB/c mouse malaria infected by P. y17XL was investigated. Female BALB/c mice at the ages of 6~8 weeks were randomly divided into vitamin （ V） treated groups and the con-trol groups. V treated groups were administered by oral gavage with 50 mg/kg VA, 600 mg/kg VE or 1 g/VC in 0.2 mL per mouse, respectively, for 10 d successively;the control groups were given the same dose of solvent （ soybean oil or saline）. Then each group of mice was intraperitoneally inoculated with 1 ＆#237;106 P. y l7XL parasitized erythro-cytes. Parasitemia levels and survival rate were dynamically observed. Flow cytometry was performed to detect the per-centage of dendritic cells subsets （ pDCs and mDCs） expression of functional molecules （ TLR9 and MHCII） at 0 d, 3 d and 5 d after the infection. The results showed that as compared with the control groups, the parasitemia levels in VA and VE treated mice was elevated, and the survival rate dampened. Splenic pDCs and mDCs were also significant-ly decreased companied with lower level of TLR9 and MHCIImolecules at 5 d after infection. In contrast, VC trea-ted mice showed reduced levels of parasitemia, with survival rate extended, and the expression of pDCs and mDCs subgroup as well as the expression levels of TLR9 and MHCIIwere significantly elevated. Therefore, it could be con-cluded that different vitamins have different regulation on malaria infection. VA and VE could promote plasmodium in-fection by inhibition of the numbers and functions of DCs and worsen the malaria infection, whereas VC could delay the infection process by promote the numbers and functions of DCs.