首页> 外文OA文献 >Toxoplasma gondii Infection of Neurons Induces Neuronal Cytokine and Chemokine Production, but Gamma Interferon- and Tumor Necrosis Factor-Stimulated Neurons Fail To Inhibit the Invasion and Growth of T. gondii
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Toxoplasma gondii Infection of Neurons Induces Neuronal Cytokine and Chemokine Production, but Gamma Interferon- and Tumor Necrosis Factor-Stimulated Neurons Fail To Inhibit the Invasion and Growth of T. gondii

机译:弓形虫感染神经元可诱导神经元细胞因子和趋化因子的产生,但γ干扰素和肿瘤坏死因子刺激的神经元不能抑制弓形虫的侵袭和生长。

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摘要

The intracellular parasite Toxoplasma gondii has the capacity to persist in the brain within neurons. In this study we demonstrated that T. gondii infected murine cerebellar neurons in vitro and replicated within these cells. Stimulation with gamma interferon (IFN-γ) and/or tumor necrosis factor (TNF) did not enable neurons to inhibit parasite invasion and replication. Cultured neurons constitutively produced interleukin 1 (IL-1), IL-6, macrophage inflammatory protein 1α (MIP-1α), and MIP-1β but not transforming growth factor β1 (TGF-β1), IL-10, and granulocyte-macrophage colony-stimulating factor. Neuronal expression of some cytokines (IL-6, TGF-β1) and chemokines (MIP-1β) was regulated by infection and/or by IFN-γ and TNF.
机译:细胞内寄生虫弓形虫具有在神经元内的大脑中持续存在的能力。在这项研究中,我们证明了弓形虫在体外感染了鼠小脑神经元并在这些细胞中复制。 γ干扰素(IFN-γ)和/或肿瘤坏死因子(TNF)刺激不能使神经元抑制寄生虫的入侵和复制。培养的神经元组成性地产生白介素1(IL-1),IL-6,巨噬细胞炎性蛋白1α(MIP-1α)和MIP-1β,但不产生转化生长因子β1(TGF-β1),IL-10和粒细胞巨噬细胞集落刺激因子。某些细胞因子(IL-6,TGF-β1)和趋化因子(MIP-1β)的神经元表达受感染和/或受IFN-γ和TNF调节。

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