干扰素-γ介导的神经元抗病毒活性的破坏：大麻素的作用。
Disruption of IFN-gamma- mediated antiviral activity in neurons: the role of cannabinoids.
作者信息
Herrera R Antonio, Oved Joseph H, Reiss Carol Shoshkes
机构信息
Department of Biology, New York University, New York, New York, USA.
出版信息
Viral Immunol. 2008 Jun;21(2):141-52. doi: 10.1089/vim.2007.0109.
Interferon-gamma (IFN-gamma) has potent antiviral activity in neurons which is affected by the production of nitric oxide (NO). This study examines the interactions between cannabinoid receptor-1 (CB(1)), IFNgamma-induced pathways, and inhibition of vesicular stomatitis virus (VSV) replication in neuronal cells. CB(1) is abundantly expressed in neurons of the CNS and the NB41A3 neuroblastoma cell line. CB(1) activation of NB41A3 cells by the synthetic cannabinoid, WIN55,212-2, is associated with an inhibition of Ca(2+) mobilization, leading to diminished nitric oxide synthase (NOS)-1 activity and the production of NO, in vitro. This ultimately results in antagonism of IFN-gamma-mediated antiviral activity and enhanced viral replication. Therefore, activation of cells expressing CB(1) by endogenous (or exogenous) ligands may contribute to decreased inflammation and to increased viral replication in neurons and disease in the CNS.
干扰素-γ（IFN-γ）在神经元中具有强大的抗病毒活性，而这种活性会受到一氧化氮（NO）产生的影响。本研究考察了大麻素受体-1（CB(1)）、IFN-γ诱导的信号通路以及对神经元细胞中水泡性口炎病毒（VSV）复制的抑制之间的相互作用。CB(1)在中枢神经系统的神经元和NB41A3神经母细胞瘤细胞系中大量表达。在体外，合成大麻素WIN55,212-2对NB41A3细胞的CB(1)激活与Ca(2+)动员的抑制相关，导致一氧化氮合酶（NOS）-1活性降低和NO产生减少。这最终导致IFN-γ介导的抗病毒活性受到拮抗，病毒复制增强。因此，内源性（或外源性）配体对表达CB(1)的细胞的激活可能导致神经元炎症减轻、病毒复制增加以及中枢神经系统疾病。
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