Watkins Linda R, Maier Steven F, Goehler Lisa E
Department of Psychology, University of Colorado at Boulder, Boulder, CO 80309, USA.
Pain. 1995 Dec;63(3):289-302. doi: 10.1016/0304-3959(95)00186-7.
It has recently become accepted that the activated immune system communicates to brain via release of pro-inflammatory cytokines. This review examines the possibility that pro-inflammatory cytokines (interleukins and/or tumor necrosis factor) mediate a variety of commonly studied hyperalgesic states. We will first briefly review basic immune responses and inflammation. We will then develop the concept of illness responses and provide evidence for their existence and for the dramatic changes in neural functioning that they cause. Lastly, we will examine the potential roles that both pro-inflammatory cytokines and the neural circuits that they activate may play in the hyperalgesic states produced by irritants, inflammatory agents, and nerve damage. The possibility is raised that apparently diverse hyperalgesic states may converge in the central nervous system and activate similar or identical neural circuitry.
最近人们已经接受，激活的免疫系统通过释放促炎细胞因子与大脑进行通信。本综述探讨了促炎细胞因子（白细胞介素和/或肿瘤坏死因子）介导各种常见的痛觉过敏状态的可能性。我们将首先简要回顾基本的免疫反应和炎症。然后我们将阐述疾病反应的概念，并为其存在以及它们所引起的神经功能的显著变化提供证据。最后，我们将研究促炎细胞因子及其激活的神经回路在由刺激物、炎症介质和神经损伤所产生的痛觉过敏状态中可能发挥的潜在作用。由此提出一种可能性，即明显不同的痛觉过敏状态可能在中枢神经系统中汇聚并激活相似或相同的神经回路。
