吗啡增加艾滋病模型海马中的病毒载量，并抑制额叶 CCL5 的表达。
Morphine increases hippocampal viral load and suppresses frontal lobe CCL5 expression in the LP-BM5 AIDS model.
机构信息
Graduate School of Biomedical Sciences and Engineering, University of Maine, Orono, ME 04473, USA; Department of Biomedical Sciences, College of Osteopathic Medicine, University of New England, Biddeford, ME 04005, USA; Center for Excellence in the Neurosciences, University of New England, Biddeford, ME 04005, USA.
Department of Biomedical Sciences, College of Osteopathic Medicine, University of New England, Biddeford, ME 04005, USA; Center for Excellence in the Neurosciences, University of New England, Biddeford, ME 04005, USA.
出版信息
J Neuroimmunol. 2014 Apr 15;269(1-2):44-51. doi: 10.1016/j.jneuroim.2014.02.010. Epub 2014 Feb 28.
Abstract
Chronic opiate abuse accelerates the development of cognitive deficits in human immunodeficiency virus (HIV)-1 patients. To investigate morphine's effects on viral infection of the central nervous system, we applied chronic morphine treatment to the LP-BM5 murine acquired immunodeficiency syndrome (MAIDS) model. LP-BM5 infection induces proinflammatory cytokine/chemokine production, correlating to increased blood-brain barrier permeability. Morphine treatment significantly increased LP-BM5 viral load in the hippocampus, but not in the frontal lobe. Morphine reduced the chemokine CCL5 to non-infected levels in the frontal lobe, but not in the hippocampus. These data indicate a region-specific mechanism for morphine's effects on virally-induced neurocognitive deficits.
摘要
慢性阿片类药物滥用加速了人类免疫缺陷病毒（HIV-1）患者认知能力下降的发展。为了研究吗啡对中枢神经系统病毒感染的影响，我们将慢性吗啡治疗应用于 LP-BM5 鼠获得性免疫缺陷综合征（MAIDS）模型。LP-BM5 感染诱导促炎细胞因子/趋化因子的产生，与血脑屏障通透性增加相关。吗啡治疗显著增加了海马体中的 LP-BM5 病毒载量，但对额叶没有影响。吗啡降低了额叶中趋化因子 CCL5 的水平，使其达到非感染水平，但对海马体没有影响。这些数据表明吗啡对病毒引起的神经认知缺陷的影响存在区域特异性机制。
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