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外围CCL2-CCR2信号有助于慢性头痛相关的敏感化

Sun Ryu¹, Xuemei Liu¹, Tingting Guo¹

¹Department of Anesthesiology and Washington University Pain Center, Washington University School of Medicine, Campus Box MSC 8054-86-05, St. Louis, MO 63110, USA.

Brain : a journal of neurology

|June 7, 2023

概括

免疫细胞中C-C动机连接体2 (CCL2) 和其受体CCR2所涉及的化学激素信号通过增强神经元敏感性,有助于慢性偏头痛. 针对CCL2-CCR2和CGRP通路提供了更有效的慢性头痛治疗方法.

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:

慢性偏头痛是一种使人衰弱的疾病,其机制尚不清楚,治疗选择有限.
三分泌血管路径与偏头痛病理生理学有关,涉及到主干神经元的激活和敏感化.
已知化学C-C动机配体2 (CCL2) 和其受体CCR2的信号传递能够调解慢性疼痛的发展.

研究的目的:

研究CCL2-CCR2信号通路在慢性偏头痛发展中的作用.
为了确定参与慢性头痛的CCL2和CCR2的细胞来源.
评估单独或与CGRP抑制结合向CCL2-CCR2通路的治疗潜力.

主要方法:

慢性头痛在小鼠中模拟使用酸甘油 (NTG) 和克制压力的重复服药.
用Ccl2和Ccr2的全球淘汰赛小鼠来评估这种途径的必要性.
他们使用了CCL2中和抗体和在特定细胞类型 (T细胞,髓状细胞,主 afferent神经元) 中基因删除CCR2.
分析了CCL2和CCR2的表达水平,以及神经元对CGRP和PACAP的反应.

主要成果:

重复的NTG给药在硬膜和三腺 (TG) 组织中提高了Ccl2和Ccr2mRNA的调节.
全球淘汰赛Ccl2和Ccr2小鼠没有产生NTG诱导的过敏,CCL2抗体治疗抑制了头痛行为.
CCR2在巨细胞和T细胞中表达,而不是TG神经元;在T细胞或骨髓细胞中消除CCR2消除了NTG诱导的行为.
在野生型但不是Ccr2淘汰赛小鼠中,NTG增加了对CGRP和PACAP的TG神经元反应.
同时使用CCL2和CGRP中和抗体在逆转头痛行为方面比单个抗体更有效.

结论:

巨细胞和T细胞中的外周CCL2-CCR2信号传递对于建立慢性头痛相关敏感性至关重要.
这一途径增强TG神经元中的CGRP和PACAP信号,导致持续的神经元敏感化.
CCL2-CCR2通路代表了慢性偏头痛的潜在治疗标,CCL2-CCR2和CGRP的联合抑制显示出增强的疗效.

关键词:

在CCL2中,我们可以使用CCL2.CCR2 是一个CCR2 的类型.头痛是一种头痛.偏头痛偏头痛偏头痛偏头痛神经免疫相互作用的相互作用周边敏感化周边敏感化

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