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Microglial STING activation alleviates nerve injury-induced neuropathic pain in male but not female miceopen access

Authors
Prudente, Arthur SilveiraLee, Sang HoonRoh, JueunLuckemeyer, Debora D.Cohen, Cinder F.Pertin, MariePark, Chul-KyuSuter, Marc R.Decosterd, IsabelleZhang, Jun -MingJi, Ru-RongBerta, Temugin
Issue Date
Mar-2024
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Keywords
Neuropathic pain; Microglia; STING; Spared nerve injury; Sex difference; Interferon; Cytokines
Citation
BRAIN BEHAVIOR AND IMMUNITY, v.117, pp 51 - 65
Pages
15
Journal Title
BRAIN BEHAVIOR AND IMMUNITY
Volume
117
Start Page
51
End Page
65
URI
https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/90509
DOI
10.1016/j.bbi.2024.01.003
ISSN
0889-1591
1090-2139
Abstract
Microglia, resident immune cells in the central nervous system, play a role in neuroinflammation and the development of neuropathic pain. We found that the stimulator of interferon genes (STING) is predominantly expressed in spinal microglia and upregulated after peripheral nerve injury. However, mechanical allodynia, as a marker of neuropathic pain following peripheral nerve injury, did not require microglial STING expression. In contrast, STING activation by specific agonists (ADU-S100, 35 nmol) significantly alleviated neuropathic pain in male mice, but not female mice. STING activation in female mice leads to increase in proinflammatory cytokines that may counteract the analgesic effect of ADU-S100. Microglial STING expression and type I interferon-ss (IFNss) signaling were required for the analgesic effects of STING agonists in male mice. Mechanistically, downstream activation of TANK-binding kinase 1 (TBK1) and the production of IFN-ss, may partly account for the analgesic effect observed. These findings suggest that STING activation in spinal microglia could be a potential therapeutic intervention for neuropathic pain, particularly in males.
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