Institute of NeuroImmune Pharmacology, Seton Hall University, 400 South Orange Ave., South Orange, NJ 07079, USA.
J Neuroimmunol. 2011 Jul;236(1-2):57-64. doi: 10.1016/j.jneuroim.2011.05.009. Epub 2011 Jun 17.
This study examined the mechanism by which exposure to lipopolysaccharide (LPS) alters mu-opioid receptor (MOR) expression in immune and neuronal cells using an in vitro conditioned medium model system. We found that LPS stimulated the intracellular accumulation of reactive oxygen species (ROS) and MOR expression in macrophage-like TPA-HL-60 cells. Conditioned medium from the LPS-stimulated TPA-HL-60 cells increased MOR expression in SH-SY5Y cells, a neuronal cell model, through actions mediated by TNF-α and GM-CSF. These data suggest that the endotoxin, LPS, modulates MOR expression in nervous and immune cells via ROS signaling, and demonstrates the crosstalk that exists within the neuroimmune axis.
本研究使用体外条件培养基模型系统，考察了脂多糖（LPS）暴露改变免疫和神经元细胞中μ-阿片受体（MOR）表达的机制。我们发现 LPS 刺激巨噬细胞样 TPA-HL-60 细胞中活性氧（ROS）的细胞内积累和 MOR 表达。来自 LPS 刺激的 TPA-HL-60 细胞的条件培养基通过 TNF-α和 GM-CSF 介导的作用增加神经元细胞模型 SH-SY5Y 细胞中的 MOR 表达。这些数据表明内毒素 LPS 通过 ROS 信号调节神经和免疫细胞中的 MOR 表达，并证明了神经免疫轴内存在的串扰。
