Cytokine/chemokine profile in J774 macrophage cells persistently infected with DA strain of Theiler's murine encephalomyelitis virus (TMEV)
Cytokine/chemokine profile in J774 macrophage cells persistently infected with DA strain of Theiler's murine encephalomyelitis virus (TMEV)
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DOI：
10.3109/13550284.2010.484040
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发表时间：
2010-06-01
影响因子：
3.2
通讯作者：
Ohara, Yoshiro
中科院分区：
文献类型：
--
作者：
Himeda, Toshiki;Okuwa, Takako;Ohara, Yoshiro
泰勒氏小鼠脑脊髓炎病毒(TMEV)是一种微小核糖核酸病毒，持续存在于小鼠的脊髓中，随后是炎症性脱髓鞘疾病。病毒持久性是TMEV诱导脱髓鞘的关键决定因素。巨噬细胞被认为是TMEV在慢性脱髓鞘阶段持续存在的部位。我们先前已经证明TMEV的两个非结构蛋白L和L-*对病毒在J774.1巨噬细胞中的生长起重要作用。然而，巨噬细胞与病毒持久性和脱髓鞘相关的关键因素仍然知之甚少。炎症反应在很大程度上依赖于免疫系统和中枢神经系统(CNS)细胞产生的细胞因子和趋化因子。在本研究中，我们建立了DA株持续感染的巨噬细胞，并分析了这些细胞中细胞因子的表达模式。本研究首次证实了DA株持续感染巨噬细胞后，B淋巴细胞趋化因子(BLC)和粒细胞集落刺激因子(G-CSF)表达上调。IL-10的表达上调，干扰素-α4、干扰素-β和干扰素-γ的表达下调。提示这些细胞因子/趋化因子可能参与了TMEV诱导的脱髓鞘过程中病毒的持续存在和脱髓鞘的加速。神经病毒学杂志(2010)16,219-229。
Theiler's murine encephalomyelitis virus (TMEV) is a picornavirus and persists in the spinal cords of mice, followed by inflammatory demyelinating disease. Viral persistence is a key determinant for the TMEV-induced demyelination. Macrophages are thought to serve as the site of TMEV persistence during the chronic demyelinating phase. We previously demonstrated that two nonstructural proteins of TMEV, L and L-*, were important for virus growth in J774.1 macrophage cells. However, the key factors of macrophage cells related to virus persistence and demyelination remain poorly understood. The inflammatory response is heavily dependent on cytokine and chemokine production by cell of both the immune system and the central nervous system (CNS). In this study, we established the macrophage cells persistently infected with DA strain, and then analyzed the cytokine expression pattern in those cells. The present results are the first to demonstrate the up-regulation of B-lymphocyte chemoattractant (BLC) and granulocyte colony-stimulating factor (G-CSF) in the macrophage cells persistently infected with DA strain. Furthermore, up-regulation of interleukin (IL)-10 and down-regulation of interferon (IFN)-alpha 4, IFN-beta, and IFN-gamma were shown in those cells. The data suggest that these cytokines/chemokines may contribute to the virus persistence and the acceleration of TMEV-induced demyelination. Journal of NeuroVirology (2010) 16, 219-229.