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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Does a neuroimmune interaction contribute to the genesis of painful peripheral neuropathies
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Does a neuroimmune interaction contribute to the genesis of painful peripheral neuropathies

机译：神经免疫相互作用是否会导致周围神经痛的发生

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摘要

Painful peripheral neuropathies are precipitated by nerve injury from disease or trauma. All such injuries will be accompanied by an inflammatory reaction, a neuritis, that will mobilize the immune system. The role of the inflammation itself is difficult to determine in the presence of structural damage to the nerve. A method has been devised to produce a focal neuritis in the rat sciatic nerve that involves no more than trivial structural damage to the nerve. This experimental focal neuritis produces neuropathic pain sensations (heat-and mechano-hyperalgesia, and cold-and mechano-allodynia) in the ipsilateral hind paw. The abnormal pain sensations begin in 1-2 days and last for 4-6 days, with a subsequent return to normal. These results suggest that there is a neuroimmune interaction that occurs at the outset of nerve injury (and perhaps episodically over time in slow developing conditions like diabetic neuropathy) that produces neuropathic pain. The short duration of the phenomena suggest that they may prime the system for more slowly developing mechanisms of abnormal pain (e.g., ectopic discharge in axotomized primary afferent neurons) that underlie the chronic phase of painful neuropathy.
机译：疾病或外伤引起的神经损伤会加剧周围神经痛。所有这些伤害都将伴随发炎反应，神经炎，从而动员免疫系统。在神经结构受损的情况下，很难确定炎症本身的作用。已经设计出一种在大鼠坐骨神经中产生局灶性神经炎的方法，该方法只对神经造成微不足道的结构损伤。这种实验性局灶性神经炎在同侧后爪产生神经性疼痛感（热和机械性痛觉过敏，以及冷和机械性痛觉过敏）。异常的疼痛感始于1-2天，持续4-6天，随后恢复正常。这些结果表明，在神经损伤开始时会发生神经免疫相互作用（可能在一段时间内在诸如糖尿病性神经病等缓慢发展的状况中随着时间而流行）产生神经性疼痛。这种现象的持续时间很短，表明它们可能会引发系统以缓慢地发展异常疼痛的机制（例如，轴突切除的初级传入神经元中的异位放电），这是疼痛性神经病的慢性阶段的基础。

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