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妊娠マウスを用いた先天性トキソプラズマ症モデルにおけるRT-PCRによるサイトカイン産生の解析

机译:妊娠マウスを用いた先天性トキソプラズマ症モデルにおけるRT-pCRによるサイトカイン产生の解析

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摘要

To explore the mechanisms of immune responses of host to Toxoplasma gondii ( T. gondii) infection in pregnant mice, we evaluated roles of cytokines [interferon gamma (IFN-y), tumor necrosis factor α (TNF-α), interleukin 6 (IL-6) and interleukin 4 (IL-4)] J by measuring mRNAS of these cytokines in placentas, lungs and spleens. The pathogenic effects of time and duration of the Fukaya infection on cytokine mRNA levels in pregnant mice were analyzed. The abundance of mRNAS encoding these cytokines was measured by reverse transcriptase (RT)-PCR at early and late stages of pregnancy in various organs of both susceptible C57BL/6 and resistant BALB/c pregnant mice infected with T. gondii. IFN-y and TNF-α but not IL-6 or IL-4, were predominant in the immune responses of placentas, lungs and spleens of BALB/ c and C57BL/6 mice during T. gondii infection. Levels of IFN-y and TNF-α mRNA in placentas of early stage pregnant BALB/c mice (infected at one-week pregnancy and examined on day 4 after infection; 1W4D) were higher than those in corresponding C57BL/6 pregnant mice, which might correlate with the fact that higher parasite numbers in placentas and lungs of C57BL/6 mice (infected at one-week pregnancy and examined on day 11 after the Fukaya infection; 1W11D) were observed than those in placentas and lungs of corresponding BALB/c mice, but not correlate with the result of parasite numbers (T. gondii No./mg tissue) in spleens of C57BL/6 (O) and BALB/c (120±56) pregnant mice. In the late stage of pregnancy, levels of IFN-y and TNF-α did not show definite correlations with T. gondii loads in placentas, lungs and spleens. These results indicate that endogenous IFN-y and TNF-α of early stage pregnancy may be essential for inhibition of T. gondii growth in some organs (placentas and lungs), but not in spleens, and the mechanisms of genetic influence involved in the susceptibility and resistance to acute T. gondii infection may include several immune responses acting together.
机译:为了探讨宿主对孕鼠弓形虫(T. gondii)感染的免疫应答机制,我们评估了细胞因子[干扰素γ(IFN-y),肿瘤坏死因子α(TNF-α),白介素6(IL)的作用。 -6)和白介素4(IL-4)] J通过测量胎盘,肺和脾中这些细胞因子的mRNAS来确定。 Fukaya感染的时间和持续时间对怀孕小鼠细胞因子mRNA水平的致病作用进行了分析。在怀孕的早期和晚期,在感染了弓形虫的易感性C57BL / 6和耐药BALB / c妊娠小鼠的各个器官中,通过逆转录酶(RT)-PCR测量了编码这些细胞因子的mRNA的丰度。在刚地弓形虫感染期间,BALB / c和C57BL / 6小鼠的胎盘,肺和脾脏的免疫反应中,IFN-γ和TNF-α而非IL-6或IL-4占主导。早期妊娠BALB / c小鼠(妊娠一周,在感染后第4天检查; 1W4D)的胎盘中IFN-γ和TNF-αmRNA的水平高于相应的C57BL / 6妊娠小鼠。可能与以下事实有关:观察到C57BL / 6小鼠(在怀孕1周时感染并在Fukaya感染后第11天检查; 1W11D)的胎盘和肺中的寄生虫数量高于相应BALB / c的胎盘和肺中的寄生虫数量小鼠,但与C57BL / 6(O)和BALB / c(120±56)妊娠小鼠脾脏中的寄生虫数量(弓形虫数量/ mg组织)结果无关。在妊娠后期,IFN-γ和TNF-α的水平与胎盘,肺和脾中刚地弓形虫的负荷没有明确的相关性。这些结果表明,早期妊娠的内源性IFN-γ和TNF-α可能对某些器官(胎盘和肺)(而非脾脏)中抑制弓形虫的生长至关重要,并且遗传敏感性的机制也与之相关。对刚地弓形虫感染的抵抗力可能包括几种共同起作用的免疫反应。

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