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首页> 外文期刊>Infection and immunity >Investigation into the Mechanism of Gamma Interferon-Mediated Inhibition of Toxoplasma gondii in Murine Astrocytes
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Investigation into the Mechanism of Gamma Interferon-Mediated Inhibition of Toxoplasma gondii in Murine Astrocytes

机译：γ-干扰素介导的弓形虫抑制鼠星形胶质细胞的机制研究

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Toxoplasma gondii is an obligate intracellular parasite that is a common opportunistic pathogen of the central nervous system in AIDS patients. Gamma interferon (IFN-γ) alone or in combination with interleukin-1 (IL-1), IL-6, or tumor necrosis factor alpha significantly inhibits the growth of T. gondii in murine astrocytes, suggesting these are important nonimmune effector cells in the brain. Inhibition was found to be independent of a nitric oxide-mediated or tryptophan starvation mechanism. Both reactive oxygen intermediates and iron deprivation are IFN-γ-mediated mechanisms known to operate against intracellular parasites in other cell types. Astrocytes generated from mice genetically deficient in the production of reactive oxygen intermediates (phox ?/?mice) were found to inhibit growth of T. gondii when stimulated with IFN-γ alone or in combination with other cytokines. The reactive oxygen inhibitor catalase and the reactive oxygen scavengers mannitol and thiourea failed to reverse the IFN-γ-induced inhibition of T. gondii in astrocytes. These data indicate that IFN-γ-induced inhibition in astrocytes is independent of reactive oxygen intermediates. IFN-γ-induced inhibition could not be reversed by the addition of iron salts, ferric citrate, ferric nitrate, or ferric transferrin. Pretreatment of astrocytes with desferrioxamine also did not induce the inhibition of T. gondii. These data indicate that the mechanism of IFN-γ inhibition was not due to iron deprivation. IFN-γ had no effect on T. gondii invasion of astrocytes, but inhibition of growth and loss of tachyzoite vacuoles were evident in IFN-γ-treated astrocytes by 24 h after invasion. Overall, these data suggest that IFN-γ-activated astrocytes inhibitT. gondii by an as-yet-unknown mechanism.
机译：弓形虫是专性的细胞内寄生虫，是艾滋病患者中枢神经系统的常见机会病原体。单独或与白介素-1（IL-1），IL-6或肿瘤坏死因子α组合使用的γ-干扰素（IFN-γ）可以显着抑制鼠星形胶质细胞中弓形虫的生长，这表明它们是重要的非免疫效应细胞。大脑。发现抑制作用独立于一氧化氮介导或色氨酸饥饿机制。活性氧中间体和铁剥夺都是干扰素-γ介导的机制，已知对其他细胞类型的细胞内寄生虫起作用。当单独用IFN-γ或与其他细胞因子联合刺激时，发现从遗传上缺乏活性氧中间体（phox /λ小鼠）产生的小鼠产生的星形胶质细胞可抑制弓形虫的生长。活性氧抑制剂过氧化氢酶和活性氧清除剂甘露醇和硫脲未能逆转IFN-γ诱导的星形胶质细胞对弓形虫的抑制作用。这些数据表明，星形胶质细胞中IFN-γ诱导的抑制作用与活性氧中间体无关。通过添加铁盐，柠檬酸铁，硝酸铁或转铁蛋白不能逆转IFN-γ诱导的抑制作用。用去铁草胺预处理星形胶质细胞也不会诱导弓形虫的抑制。这些数据表明，IFN-γ抑制的机制不是由于铁缺乏。 IFN-γ对刚地弓形虫侵袭星形胶质细胞没有影响，但是在IFN-γ处理的星形胶质细胞侵袭后24小时，其生长抑制和速殖子空泡的丧失是明显的。总的来说，这些数据表明IFN-γ激活的星形胶质细胞抑制T。刚迪通过一种未知的机制。

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