Neuropathic pain and cytokines: current perspectives.
Neuropathic pain and cytokines: current perspectives.
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DOI：
10.2147/jpr.s53660
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发表时间：
2013
影响因子：
2.7
通讯作者：
Malcangio M
中科院分区：
文献类型：
--
作者：
Clark AK;Old EA;Malcangio M
神经性疼痛代表临床医学中的主要问题，因为它引起使人衰弱的痛苦并且在很大程度上对当前可用的镇痛剂具有抗性。神经性疼痛的一个特征是对躯体感觉刺激的异常反应。因此，患有周围神经病的患者可能会经历由通常不痛的刺激引起的疼痛，例如皮肤的简单触摸或温度变化，以及对有害刺激的过度反应。令人信服的证据表明，这种超敏反应是疼痛保持集中的结果。特别是，在脊髓背角的第一个疼痛突触处，神经元的增益增加，神经元开始被无害的输入激活。近年来，人们已经认识到，外周神经系统的远程损伤导致神经元可塑性和小胶质细胞和星形胶质细胞活性的变化，以及巨噬细胞和T细胞的浸润，这些都有助于中枢致敏。具体地，从神经元和非神经元细胞释放诸如细胞因子和趋化因子的原伤害感受因子可以使第一疼痛突触的神经元敏感。在这篇文章中，我们回顾了目前的证据，细胞因子介导的脊髓神经元-非神经元细胞通讯的神经病理性疼痛机制后，周围神经损伤的作用。特异性和选择性地控制马槟榔碱介导的神经元-神经胶质细胞相互作用导致在神经病理性疼痛模型中观察到的对有害和无害刺激的超敏反应减弱，并且可能代表未来治疗干预的途径。
Neuropathic pain represents a major problem in clinical medicine because it causes debilitating suffering and is largely resistant to currently available analgesics. A characteristic of neuropathic pain is abnormal response to somatic sensory stimulation. Thus, patients suffering peripheral neuropathies may experience pain caused by stimuli which are normally nonpainful, such as simple touching of the skin or by changes in temperature, as well as exaggerated responses to noxious stimuli. Convincing evidence suggests that this hypersensitivity is the result of pain remaining centralized. In particular, at the first pain synapse in the dorsal horn of the spinal cord, the gain of neurons is increased and neurons begin to be activated by innocuous inputs. In recent years, it has become appreciated that a remote damage in the peripheral nervous system results in neuronal plasticity and changes in microglial and astrocyte activity, as well as infiltration of macrophages and T cells, which all contribute to central sensitization. Specifically, the release of pronociceptive factors such as cytokines and chemokines from neurons and non-neuronal cells can sensitize neurons of the first pain synapse. In this article we review the current evidence for the role of cytokines in mediating spinal neuron–non-neuronal cell communication in neuropathic pain mechanisms following peripheral nerve injury. Specific and selective control of cytokine-mediated neuronal–glia interactions results in attenuation of the hypersensitivity to both noxious and innocuous stimuli observed in neuropathic pain models, and may represent an avenue for future therapeutic intervention.