Peripheral Neuroimmune Interactions and Neuropathic Pain

Peripheral Neuroimmune Interactions and Neuropathic Pain
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周围神经免疫相互作用和神经性疼痛

DOI:
10.1007/978-1-4939-1071-7_6
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发表时间:
2014
期刊:
影响因子:
--
通讯作者:
Machelska H
Machelska H
中科院分区:
--
文献类型:
--
作者:
Machelska H

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神经性疼痛通常由周围神经损伤引起,这可以动员免疫系统,如格林-巴利综合征,带状疱疹后神经痛或创伤。虽然大多数研究集中在神经炎症的有害影响,最近的实验数据提供证据的镇痛作用的白细胞。疼痛改善作用涉及抗炎细胞因子和免疫细胞衍生的阿片肽,其激活受损神经中感觉神经元外周末梢上的阿片受体。此外,内源性大麻素存在于白细胞中,并且参与炎症消退的机制已经建立,但它们对神经性疼痛调节的意义尚待研究。临床证据不太令人信服,尽管在某些情况下,疼痛的发生似乎与巨噬细胞或T淋巴细胞数量减少有关。本章讨论了神经炎症在疼痛性神经病变调节中的不利和有益作用。
Neuropathic pain often results from damage to peripheral nerves, which can mobilize the immune system, as in Guillain-Barré syndrome, postherpetic neuralgia, or trauma. Although most studies focused on detrimental effects of neuroinflammation, recent experimental data provide evidence on analgesic effects of leukocytes. Pain-ameliorating actions involve anti-inflammatory cytokines and immune cell-derived opioid peptides, which activate opioid receptors on peripheral terminals of sensory neurons in injured nerves. In addition, endocannabinoids are present in leukocytes, and mechanisms involved in the resolution of inflammation are mounted, but their significance to neuropathic pain modulation is yet to be examined. Clinical evidence is less compelling, although in some conditions the occurrence of pain seems to be associated with lowered numbers of macrophages or T lymphocytes. This chapter discusses studies addressing both unfavorable and beneficial actions of neuroinflammation in the regulation of painful neuropathies.
DOI: 10.2741/s16
发表时间: 2009-06-01
期刊: Frontiers in bioscience (Scholar edition)
影响因子: --
作者:
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通讯作者: Kraus, Jurgen
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DOI: 10.1016/s0304-3940(99)00450-4
发表时间: 1999
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