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炎症诱导的巨细胞衍生的神经生长因子:慢性疼痛的关键因素?

Yaseen Awad-Igbaria^1,2, Doron Edelman³, Elvira Ianshin⁴

¹Azrieli Faculty of Medicine, Bar-Ilan University, Safed 1311502, Israel.

Brain : a journal of neurology

|July 13, 2024

概括

炎症通过增加巨细胞和神经芽引起部疼痛. 在炎症期间准神经生长因子 (NGF) 途径可以通过减少神经元变化来预防这种疼痛.

科学领域:

神经科学是一个神经科学.
免疫学免疫学免疫学
疼痛研究疼痛研究

背景情况:

诱发性 (PV) 涉及与炎症,乳腺细胞 (MC) 积累和神经元发芽相关的慢性痛.
连接炎与神经元变化和导致过敏的脊髓适应的精确机制尚不清楚.

研究的目的:

调查炎炎引起的过敏和刺激性痛 (PV) 中的疼痛背后的机制.
探索神经生长因子 (NGF) 途径和巨细胞活性在PV发育和潜在治疗点中的作用.

主要方法:

来自有和没有PV的女性的组织的比较分析.
一种PV的动物模型,涉及反复的膜囊炎引起的炎症.
评估巨细胞积累,神经元发芽,疼痛通道表达 (TRPV1,TRPA1) 和脊髓/背部根腺 (DRG) 中的基因表达.
药理干预使用基托烟酸 (KF) 来稳定巨细胞和NGF抑制剂 (Ro08-2750).

主要成果:

在PV中, Vulvar组织显示了巨细胞和神经元发芽的增加.
在动物中,重复的炎导致长期的过敏,由巨细胞,神经元发芽和脊髓疼痛通道/基因表达改变的介导.
基托芬酸盐 (KF) 治疗减弱了巨细胞活性,降低了NGF和基因组胺水平,并通过调节神经元和脊髓变化来预防过敏.
阻断NGF活动还通过调节神经可塑性和神经元发芽来降低过敏性.

结论:

在PV中, Vulvar Allodynia是由炎症诱导的巨细胞积累,神经元发芽和 vulva 中的神经调节驱动的.
慢性部疼痛涉及脊髓中的长期基因表达适应,有助于中心敏感化.
在炎症期间调节NGF通路对于通过调节前庭和脊髓的神经元变化来预防PV至关重要,这突显了它在PV病原发生中的基本作用.

关键词:

中央敏感化中心这是一种炎症炎症炎症炎症.巨细胞 (MC) 是一种巨细胞.神经生长因子 (NGF)神经元的超内内转变引起的 (PV)

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