弓形虫对神经元的感染会诱导神经元产生细胞因子和趋化因子，但γ干扰素和肿瘤坏死因子刺激的神经元无法抑制弓形虫的侵袭和生长。
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.
作者信息
Schlüter D, Deckert M, Hof H, Frei K
机构信息
Institut für Medizinische Mikrobiologie und Hygiene, Universitätsklinikum Mannheim, Universität Heidelberg, Mannheim, Germany.
出版信息
Infect Immun. 2001 Dec;69(12):7889-93. doi: 10.1128/IAI.69.12.7889-7893.2001.
Abstract
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-gamma) 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 1alpha (MIP-1alpha), and MIP-1beta but not transforming growth factor beta1 (TGF-beta1), IL-10, and granulocyte-macrophage colony-stimulating factor. Neuronal expression of some cytokines (IL-6, TGF-beta1) and chemokines (MIP-1beta) was regulated by infection and/or by IFN-gamma and TNF.
摘要
细胞内寄生虫刚地弓形虫能够在神经元内寄生于大脑中。在本研究中，我们证明刚地弓形虫可在体外感染小鼠小脑神经元并在这些细胞内复制。用γ干扰素（IFN-γ）和/或肿瘤坏死因子（TNF）刺激并不能使神经元抑制寄生虫的侵袭和复制。培养的神经元组成性地产生白细胞介素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。一些细胞因子（IL-6、TGF-β1）和趋化因子（MIP-1β）的神经元表达受感染和/或IFN-γ及TNF调控。
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