Halonen S K, Chiu F, Weiss L M
Departments of Neurology, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
Infect Immun. 1998 Oct;66(10):4989-93. doi: 10.1128/IAI.66.10.4989-4993.1998.
Cytokines play a significant role in the regulation of Toxoplasma gondii in the central nervous system. Cytokine-activated microglia are important host defense cells in central nervous system infections. Recent evidence indicates that astrocytes can also be activated by cytokines to inhibit intracellular pathogens. In this study, we examined the effect of gamma interferon (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6), and IL-1 on the growth of T. gondii in a primary murine astrocyte culture. Pretreatment of astrocytes with IFN-gamma resulted in 65% inhibition of T. gondii growth. Neither TNF-alpha, IL-1, nor IL-6 alone had any effect on T. gondii growth. IFN-gamma in combination with either TNF-alpha, IL-1, or IL-6 caused a 75 to 80% inhibition of growth. While nitric oxide was produced by astrocytes treated with these cytokines, inhibition of T. gondii growth was not reversed by the addition of the nitric oxide synthase inhibitor NG-monomethyl-L-arginine. Furthermore, IFN-gamma in combination with IL-1, IL-6, or TNF-alpha also induced inhibition in astrocytes derived from syngeneic mice deficient in the enzyme inducible nitric oxide synthase. This finding suggests that the mechanism of cytokine inhibition is not nitric oxide mediated. Similarly, the addition of tryptophan had no effect on inhibition, indicating that the mechanism was not mediated via induction of the enzyme indoleamine 2, 3-dioxygenase. The mechanism of inhibition remains to be elucidated. Results from this study demonstrate that cytokine-activated astrocytes are capable of significantly inhibiting the growth of T. gondii. These data indicate that astrocytes may be important host defense cells in controlling toxoplasmosis in the brain.
细胞因子在中枢神经系统中弓形虫的调控中发挥着重要作用。细胞因子激活的小胶质细胞是中枢神经系统感染中重要的宿主防御细胞。最近的证据表明,星形胶质细胞也可被细胞因子激活以抑制细胞内病原体。在本研究中,我们检测了γ干扰素(IFN-γ)、肿瘤坏死因子α(TNF-α)、白细胞介素-6(IL-6)和IL-1对原代小鼠星形胶质细胞培养物中弓形虫生长的影响。用IFN-γ预处理星形胶质细胞可导致弓形虫生长受到65%的抑制。单独的TNF-α、IL-1或IL-6对弓形虫生长均无任何影响。IFN-γ与TNF-α、IL-1或IL-6联合使用可导致75%至80%的生长抑制。虽然这些细胞因子处理的星形胶质细胞会产生一氧化氮,但添加一氧化氮合酶抑制剂NG-甲基-L-精氨酸并不能逆转对弓形虫生长的抑制。此外,IFN-γ与IL-1、IL-6或TNF-α联合使用也可在缺乏诱导型一氧化氮合酶的同基因小鼠来源的星形胶质细胞中诱导抑制作用。这一发现表明细胞因子抑制机制不是由一氧化氮介导的。同样,添加色氨酸对抑制作用也无影响,表明该机制不是通过诱导吲哚胺2,3-双加氧酶介导的。抑制机制仍有待阐明。本研究结果表明,细胞因子激活的星形胶质细胞能够显著抑制弓形虫的生长。这些数据表明,星形胶质细胞可能是控制脑部弓形虫病的重要宿主防御细胞。