CCR2介导因暴露于HIV-1反式激活因子（Tat）和阿片类物质而导致的神经胶质激活增加。
CCR2 mediates increases in glial activation caused by exposure to HIV-1 Tat and opiates.
作者信息
El-Hage Nazira, Wu Guanghan, Ambati Jayakrishna, Bruce-Keller Annadora J, Knapp Pamela E, Hauser Kurt F
机构信息
Department of Anatomy and Neurobiology, University of Kentucky Medical Center, Lexington, KY 40536, USA.
出版信息
J Neuroimmunol. 2006 Sep;178(1-2):9-16. doi: 10.1016/j.jneuroim.2006.05.027. Epub 2006 Jul 10.
Abstract
To assess the role of CCL2/MCP-1 in opiate drug abuse and HIV-1 comorbidity, the effects of systemic morphine and intrastriatal HIV-1 Tat on macrophage/microglial and astroglial activation were assessed in wild type and CCR2 null mice. Tat and/or morphine additively increased the proportion of CCL2 immunoreactive astroglia. The effects of morphine were prevented by naltrexone. Glial activation was significantly reduced in CCR2-/- versus wild-type mice following Tat or morphine plus Tat exposure. Thus, CCR2 contributes to local glial activation caused by Tat alone or in the presence of opiates, implicating CCR2 signaling in HIV-1 neuropathogenesis in drug abusers and non-abusers.
摘要
为评估CCL2/MCP-1在阿片类药物滥用和HIV-1合并症中的作用，在野生型和CCR2基因敲除小鼠中评估了全身注射吗啡和纹状体内注射HIV-1反式激活因子（Tat）对巨噬细胞/小胶质细胞和星形胶质细胞激活的影响。Tat和/或吗啡可累加增加CCL2免疫反应性星形胶质细胞的比例。纳曲酮可阻断吗啡的作用。在暴露于Tat或吗啡加Tat后，CCR2基因敲除小鼠的胶质细胞激活明显低于野生型小鼠。因此，CCR2参与了由Tat单独或在存在阿片类药物时引起的局部胶质细胞激活，提示CCR2信号传导在吸毒者和非吸毒者的HIV-1神经病变中起作用。
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