Department of Neural and Pain Sciences, Dental School & Program in Neuroscience, University of Maryland, Baltimore, Maryland, USA.
Nat Med. 2010 Nov;16(11):1267-76. doi: 10.1038/nm.2234. Epub 2010 Oct 14.
Immune cells and glia interact with neurons to alter pain sensitivity and to mediate the transition from acute to chronic pain. In response to injury, resident immune cells are activated and blood-borne immune cells are recruited to the site of injury. Immune cells not only contribute to immune protection but also initiate the sensitization of peripheral nociceptors. Through the synthesis and release of inflammatory mediators and interactions with neurotransmitters and their receptors, the immune cells, glia and neurons form an integrated network that coordinates immune responses and modulates the excitability of pain pathways. The immune system also reduces sensitization by producing immune-derived analgesic and anti-inflammatory or proresolution agents. A greater understanding of the role of the immune system in pain processing and modulation reveals potential targets for analgesic drug development and new therapeutic opportunities for managing chronic pain.
免疫细胞和神经胶质细胞与神经元相互作用,改变疼痛敏感性,并介导急性疼痛向慢性疼痛的转变。在受伤时,常驻免疫细胞被激活,血液来源的免疫细胞被招募到损伤部位。免疫细胞不仅有助于免疫保护,还启动了外周伤害感受器的敏化。通过合成和释放炎症介质,并与神经递质及其受体相互作用,免疫细胞、神经胶质细胞和神经元形成一个整合的网络,协调免疫反应并调节疼痛通路的兴奋性。免疫系统还通过产生免疫源性的镇痛、抗炎或促解决介质来减少敏化。更深入地了解免疫系统在疼痛处理和调节中的作用,揭示了开发镇痛药物的潜在靶点和管理慢性疼痛的新治疗机会。