洛桑联邦理工Stphanie P. Lacour、苏黎世理工Qiuting Huang和哈佛医学院/波士顿儿童医院Clifford J. Woolf研究组，通过光遗传学研究发现激活伤害感受器能够启动和放大炎症。 该研究于2020年9月21日发表于《自然—生物技术》。

研究人员报告了一种神经技术，用于选择性神经外膜光遗传学（epineural optogentic）神经调节伤害感受器，并证明伤害感受器激活会驱动保护性疼痛行为和炎症。无线光电系统由亚毫米级发光二极管组成，该发光二极管嵌在柔软的周围神经坐骨神经植入物中，由微型头戴式控制单元供电和驱动。在自由移动、只在伤害感受器表达channelrhodopsin的老鼠上，光刺激神经元轴突会导致疼痛的行为特征，反映出顺行的脊髓的输入。

在没有炎症的情况下，它还会导致皮肤中的免疫反应，并且由于伤害感受器周围末端的抗皮肤活化，导致已建立的炎症得到加强。这些结果揭示了伤害感受器和免疫细胞之间的联系，可能对于炎症治疗产生影响。

据了解，通过有害刺激激活伤害感受器会同时引起疼痛以及感觉神经元的毛细血管通透性和血液流动的增加，产生神经源性炎症。然而，伤害感受器是否也与免疫系统相互作用仍知之甚少。

附：英文原文

Title: Epineural optogenetic activation of nociceptors initiates and amplifies inflammation

Author: Frdric Michoud, Corey Seehus, Philipp Schnle, No Brun, Daniel Taub, Zihe Zhang, Aakanksha Jain, Ivan Furfaro, Outman Akouissi, Rachel Moon, Pascale Meier, Katia Galan, Benjamin Doyle, Michael Tetreault, Sbastien Talbot, Liam E. Browne, Qiuting Huang, Clifford J. Woolf, Stphanie P. Lacour

Issue&Volume: 2020-09-21

Abstract: Activation of nociceptor sensory neurons by noxious stimuli both triggers pain and increases capillary permeability and blood flow to produce neurogenic inflammation1,2, but whether nociceptors also interact with the immune system remains poorly understood. Here we report a neurotechnology for selective epineural optogenetic neuromodulation of nociceptors and demonstrate that nociceptor activation drives both protective pain behavior and inflammation. The wireless optoelectronic system consists of sub-millimeter-scale light-emitting diodes embedded in a soft, circumneural sciatic nerve implant, powered and driven by a miniaturized head-mounted control unit. Photostimulation of axons in freely moving mice that express channelrhodopsin only in nociceptors resulted in behaviors characteristic of pain, reflecting orthodromic input to the spinal cord. It also led to immune reactions in the skin in the absence of inflammation and potentiation of established inflammation, a consequence of the antidromic activation of nociceptor peripheral terminals. These results reveal a link between nociceptors and immune cells, which might have implications for the treatment of inflammation. 

DOI: 10.1038/s41587-020-0673-2

Source: https://www.nature.com/articles/s41587-020-0673-2