Mata Marina, Hao Shuanglin, Fink David J
Department of Neurology, University of Michigan, 1914 Taubman Center, 1500 E. Medical Center Drive, Ann Arbor, MI 48109-0316, USA; VA Ann Arbor Healthcare System, Ann Arbor, MI 48109-0316, USA.
Neurosci Lett. 2008 Jun 6;437(3):209-13. doi: 10.1016/j.neulet.2008.03.049. Epub 2008 Mar 22.
Identification that neuroimmune activation in the spinal cord is an important factor in the development of chronic pain has opened the possibility that gene transfer of anti-inflammatory peptides may be used to reduce pain neurotransmission. We review the published evidence regarding gene transfer to meninges to express the anti-inflammatory peptide interleukin 10, and gene transfer to dorsal root ganglia using replication incompetent HSV vectors to express interleukin 4, interleukin 10, or the soluble (p55) tumor necrosis factor receptor (sTNFR). The results of these experiments suggest a novel role for "reverse signaling" through the full-length membrane form of TNFalpha in spinal glia in the modulation of chronic pain.
脊髓中的神经免疫激活是慢性疼痛发展的一个重要因素，这一发现使得通过抗炎肽的基因转移来减少疼痛神经传递成为可能。我们回顾了已发表的关于向脑膜进行基因转移以表达抗炎肽白细胞介素10，以及使用无复制能力的单纯疱疹病毒载体向背根神经节进行基因转移以表达白细胞介素4、白细胞介素10或可溶性（p55）肿瘤坏死因子受体（sTNFR）的证据。这些实验结果表明，通过脊髓神经胶质细胞中全长膜形式的肿瘤坏死因子α的“反向信号传导”在慢性疼痛调节中具有新的作用。
