Activation of nociceptor sensory neurons by noxious stimuli both triggers pain and increases capillary permeability and blood flow to produce neurogenic inflammation^1,2, 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.

伤害性刺激激活伤害感受器感觉神经元既触发疼痛，又增加毛细血管通透性和血流量，产生神经性炎症^1,2，但伤害感受器是否也与免疫系统相互作用尚不清楚。在这里，我们报告了一种针对伤害感受器的选择性神经外膜光遗传学神经调节的神经技术，并证明伤害感受器的激活既可以驱动保护性疼痛行为，又可以驱动炎症。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。仅在伤害感受器中表达通道视紫红质的自由移动小鼠中轴突的光刺激导致疼痛行为特征，反映了脊髓的矫正输入。在没有炎症的情况下，它还会导致皮肤产生免疫反应，并增强已确定的炎症，伤害感受器外围终端的反皮肤激活的结果。这些结果揭示了伤害感受器与免疫细胞之间的联系，这可能对炎症的治疗有影响。