初级感觉神经元与巨噬细胞的交互作用在痛觉敏化中的作用

Effect of cross-talk between primary sensory neuron and macrophage on hyperalgesia

急性疼痛是由伤害性感受器激活引起的一种保护机体的反应,相比之下,慢性疼痛通常作为炎症性疾病的临床症状出现,逐渐发展为中枢敏化或外周敏化。目前普遍认为免疫系统对慢性疼痛的发生与维持有重要影响。神经损伤后,免疫系统的巨噬细胞与痛觉感受器进行双向通信在疼痛的发病机制中起重要作用,具体表现为组织常驻巨噬细胞的增殖、外周巨噬细胞的浸润以及周围和中枢神经系统中炎症介质的产生。文章重点介绍了介导初级感觉神经元与背根神经节(dorsal root ganglia,DRG)内巨噬细胞相互作用的分子,以及近期出现的治疗痛觉敏化新靶点,如P物质(substance P,SP)、血管紧张素Ⅱ受体(type 2 angiotensinⅡreceptor,AT_(2)R)、微RNA(microRNA,miRNA)以及外泌体,为痛觉敏化的治疗提供新思路。

Acute pain is a protection for organisms caused by the activation of primary nociceptors,while chronic pain is a condition that often emerges as a clinical symptom of inflammatory diseases and tends to develop into central or peripheral sensitization.It has been widely accepted that the immune system critically contributes to the occurrence and maintenance of hyperalgesia.Cross-talk between macrophages and nociceptor sensory neurons is vital for the pathogenesis of pain,characterized by the proliferation of tissue-resident macrophages,infiltration of peripheral macrophages,and secretion of inflammatory mediators in the peripheral and central nervous systems.The article examines the molecules involved in the interaction between macrophages in dorsal root ganglia(DRG)and primary nociceptors,as well as recently emerging targets,including substance P(SP),type 2 angiotensinⅡreceptor(AT_(2)R),microRNA(miRNA),and exosomes,in order to provide novel ideas for the treatment of hyperalgesia.