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Lentinan treatment of Plasmodium yoelii-infected mice induces apoptosis of regulatory T cells

机译:Lentinan治疗疟原虫感染的小鼠诱导调控性T细胞的凋亡

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To determine the immunomodulatory effects of lentinan, particularly on immune-suppressing regulatory T cells (Treg), in a mouse model of malaria, BALB/c mice were infected with?Plasmodium yoelii?by intraperitoneal (i.p.) injection of?1 × 106?red blood cells containing Py17XL, and the infected mice were randomized into either a control group for i.p. injection of PBS or an experiment group for i.p. injection of lentinan. The results show that mean survival was significantly longer for infected mice treated with lentinan (8.10 ± 2.53 days) than for infected controls treated with PBS (5.20 ± 1.20 days;?P<0.01). Further, IL-12 and IFN-g?expression in spleen cells were significantly higher in the experiment group than the control group (P<0.01). When Treg cells were isolated by CD antibody detection from peripheral blood, a higher proportions were undergoing apoptosis in the experiment group than those in the control group (P<0.001). To determine the mechanism of cell death in Tregs, we analyzed Bax and Bcl-2 expression. Bax was detected at significantly higher levels, while Bcl-2 was significantly lower in Treg cells from lentinan-treated animals (P<0.001). In conclusion,?lentinan significantly delayed progression of?P. yoeliiinfection in mice by up-regulating anti-inflammatory cytokines and triggering apoptosis of Treg cells through up-regulation of Bax and down-regulation of Bcl-2, and which should be suggested in the clinical experience in the future.
机译:为了确定Lentinan的免疫调节作用,特别是在免疫抑制调节性T细胞(Treg)上,在疟疾的小鼠模型中,Balb / C小鼠感染了yoelii?通过腹膜内(IP)注射1×106?含有Py17x1的红细胞,并将感染的小鼠随机化为IP的对照组注射PBS或实验组的i.P.注射香菇。结果表明,用Lentinan(8.10±2.53天)处理的感染小鼠比用PBS处理的感染对照(5.20±1.20天;ΔP<0.01),对感染的小鼠的平均存活率明显更长。此外,实验组在实验组中的IL-12和IFN-G?在实验组中显着高于对照组(P <0.01)。当通过从外周血的CD抗体检测分离Treg细胞时,实验组在实验组中凋亡较高的比例(P <0.001)。为了确定Tregs中细胞死亡的机制,我们分析了BAX和BCL-2表达。在较高水平的水平下检测到Bax,而Bcl-2在一对必要的动物的Treg细胞中显着降低(P <0.001)。总之,?Lentinan显着延迟进展?p。通过对抗炎细胞因子进行umeliiiInfection,通过对Bcl-2的抑制和下调的预定调节引发Treg细胞凋亡,并在未来的临床经验中提出。

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