Inflammation in dorsal root ganglia after peripheral nerve injury: Effects of the sympathetic innervation
Inflammation in dorsal root ganglia after peripheral nerve injury: Effects of the sympathetic innervation
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DOI：
10.1016/j.autneu.2013.12.009
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发表时间：
2014-05-01
影响因子：
2.7
通讯作者：
Hu, Ping
中科院分区：
文献类型：
--
作者：
McLachlan, Elspeth M.;Hu, Ping
周围神经损伤后，交感神经节和背根神经节（DRGs）发生无菌炎症，其轴突在受损的神经干中突出。巨噬细胞和t淋巴细胞侵入这些神经节，在那里它们被认为释放细胞因子，导致过度兴奋和异位放电，可能导致神经性疼痛。在这里，我们研究了交感神经支配在Wistar大鼠坐骨神经横断后L5 DRGs炎症中的作用，比较了神经病变前10-14天特异性手术干预与慢性肾上腺素能受体拮抗剂治疗的效果。坐骨横断后第7天采用免疫组化法测定侵袭性免疫细胞群。通过切断相关腰椎交感神经节的节前输入（单侧或双侧分散）或通过同侧切除这些神经节伴节后轴突变性（去神经支配）来消除后肢的交感神经活动，引起的DRG炎症比假交感神经切除术后发生的炎症少。相反，引流病变部位的淋巴结去神经支配增强了t细胞的内流。全身使用α(1)-肾上腺素受体拮抗剂（吡唑嗪）或β -肾上腺素受体拮抗剂（心得安）对坐骨横断后DRGs的浸润产生相反但意想不到的影响。普拉唑嗪增强了巨噬细胞和CD4(+) t淋巴细胞的内流，而心得安则倾向于减少免疫细胞的侵袭。这些数据很难与许多体外研究相一致，在这些研究中，儿茶酚胺主要通过β(2)-肾上腺素受体起作用，抑制炎症攻击后免疫细胞的激活和增殖。(C) 2013 Elsevier B.V.版权所有
Following a peripheral nerve injury, a sterile inflammation develops in sympathetic and dorsal root ganglia (DRGs) with axons that project in the damaged nerve trunk. Macrophages and T-lymphocytes invade these ganglia where they are believed to release cytokines that lead to hyperexcitability and ectopic discharge, possibly contributing to neuropathic pain. Here, we examined the role of the sympathetic innervation in the inflammation of L5 DRGs of Wistar rats following transection of the sciatic nerve, comparing the effects of specific surgical interventions 10-14 days prior to the nerve lesion with those of chronic administration of adrenoceptor antagonists. Immunohistochemistry was used to define the invading immune cell populations 7 days after sciatic transection. Removal of sympathetic activity in the hind limb by transecting the preganglionic input to the relevant lumbar sympathetic ganglia (ipsi- or bilateral decentralization) or by ipsilateral removal of these ganglia with degeneration of postganglionic axons (denervation), caused less DRG inflammation than occurred after a sham sympathectomy. By contrast, denervation of the lymph node draining the lesion site potentiated T-cell influx. Systemic treatment with antagonists of alpha(1)-adrenoceptors (prazosin) or beta-adrenoceptors (propranolol) led to opposite but unexpected effects on infiltration of DRGs after sciatic transection. Prazosin potentiated the influx of macrophages and CD4(+) T-lymphocytes whereas propranolol tended to reduce immune cell invasion. These data are hard to reconcile with many in vitro studies in which catecholamines acting mainly via beta(2)-adrenoceptors have inhibited the activation and proliferation of immune cells following an inflammatory challenge. (C) 2013 Elsevier B.V. All rights reserved.