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

作     者：Wolfgang Liedtke Wolfgang Liedtke

作者机构：Department of NeurologyDuke University School of MedicineDurhamNC 27710USA Department of AnesthesiologyDuke University School of MedicineDurhamNC 27710USA Department of NeurobiologyDuke University School of MedicineDurhamNC 27710USA Duke Neurology Clinics for HeadacheHead-Pain and Trigeminal Sensory DisordersDurhamNC 27705USA Clinics for Innovative Pain TherapyDepartment of AnesthesiologyDuke UniversityRaleighNC 27512USA Chair of NeurologyGlobal Scientific Development CouncilRegeneron PharmaceuticalsTarrytownNY 10591USA 

出 版 物：《Neuroscience Bulletin》 (神经科学通报（英文版）)

年 卷 期：2021年第37卷第7期

页      面：1075-1078页

核心收录：

学科分类：1002[医学-临床医学] 100204[医学-神经病学] 10[医学] 

主　　题：inflammatory interferon rigorous 

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,4STING controls nociception via type-I interferon signaling in sensory neurons^,is noteworthy in this respect[3].In this paper,Donnelly et *** 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.