STING-ing Pain:How Can Pro-inflammatory Signaling Attenuate Pain?  

作　　者：Wolfgang Liedtke 

机构地区：[1]Department of Neurology,Duke University School of Medicine,Durham,NC 27710,USA [2]Department of Anesthesiology,Duke University School of Medicine,Durham,NC 27710,USA [3]Department of Neurobiology,Duke University School of Medicine,Durham,NC 27710,USA [4]Duke Neurology Clinics for Headache,Head-Pain and Trigeminal Sensory Disorders,Durham,NC 27705,USA [5]Clinics for Innovative Pain Therapy,Department of Anesthesiology,Duke University,Raleigh,NC 27512,USA [6]Chair of Neurology,Global Scientific Development Council,Regeneron Pharmaceuticals,Tarrytown,NY 10591,USA

出　　处：《Neuroscience Bulletin》2021年第7期1075-1078,共4页神经科学通报（英文版）

摘　　要：Inflammation typically induces pain by producing pro-inflammatory mediators,but increasing evidence also indicates a role for inflammation in the resolution of pain by inducing anti-inflammatory and pro-resolution mediators[1,2].A recent Nature paper from Duke University,4<STING controls nociception via type-I interferon signaling in sensory neurons^,is noteworthy in this respect[3].In this paper,Donnelly et al.from Ru-Rong JiJs lab report that activation of the STING(stimulator of interferon genes)signaling mechanism in nociceptive primary sensory neurons functions in an analgesic manner in naive and injured mice,using STING agonists,and applying sophisticated pain behavioral metrics to uninjured mice and mice with nerve constriction injury or a rigorous model of bone cancer pain.

关 键 词：INFLAMMATORY INTERFERON rigorous 

分 类 号：R741[医药卫生—神经病学与精神病学]