Sommer C
Neurologische Universitätsklinik, Josef-Schneider-Strasse 11, 97080 Würzburg.
Anaesthesist. 2001 Jun;50(6):416-26. doi: 10.1007/s001010100135.
Cytokines are a heterogeneous group of polypeptides that were originally described to mediate activation of the immune system and inflammatory responses. Most of them have meanwhile been shown to be also produced by and act on the peripheral and central nervous system. There is ample evidence from experimental studies that proinflammatory cytokines induce or increase neuropathic pain as well as inflammatory pain. Direct actions of cytokines on afferent nerve fibers have been shown as well as actions involving further mediators such as prostaglandins or nerve growth factor. Inhibition of proinflammatory cytokines, either by synthesis inhibitors, inhibitors of cleavage from the cell membrane, by direct antagonists, or by anti-inflammatory antibodies, reduces pain and hyperalgesia in most models studied. Studies with cytokine knock-out animals often lead to different results from the pharmacological studies. This is in part due to compensatory mechanisms in the animals combined with the high redundancy of the cytokine system. Preliminary data from human studies are encouraging insofar as in the future, cytokine inhibition may add to the panel of treatment modalities for neuropathic pain.
细胞因子是一类异质性多肽,最初被描述为介导免疫系统激活和炎症反应。与此同时,大多数细胞因子已被证明也由外周和中枢神经系统产生并作用于该系统。实验研究有充分证据表明,促炎细胞因子可诱导或加剧神经性疼痛以及炎性疼痛。细胞因子对传入神经纤维的直接作用以及涉及前列腺素或神经生长因子等其他介质的作用均已得到证实。在大多数研究模型中,通过合成抑制剂、细胞膜裂解抑制剂、直接拮抗剂或抗炎抗体抑制促炎细胞因子,可减轻疼痛和痛觉过敏。细胞因子基因敲除动物的研究结果往往与药理学研究结果不同。部分原因是动物体内的代偿机制以及细胞因子系统的高度冗余性。来自人体研究的初步数据令人鼓舞,因为未来细胞因子抑制可能会增加神经性疼痛的治疗方式。