Inflammasome mediated neuroinflammation as a novel target of chronic pain

2017 Fiscal Year Final Research Report

• Project/Area Number: 15H04969
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Anesthesiology
• Research Institution: Kyoto Prefectural University of Medicine
• Principal Investigator: Fumimasa Amaya 京都府立医科大学, 医学(系)研究科(研究院), 准教授 (60347466)
• Co-Investigator(Kenkyū-buntansha): 岡林 志帆子 京都府立医科大学, 医学部附属病院, 研究員 (00744898) ; 佐和 貞治 京都府立医科大学, 医学(系)研究科(研究院), 教授 (10206013) ; 大橋 憲太郎 岐阜大学, 工学部, 准教授 (50332953) ; 澤田 麻衣子 京都府立医科大学, 医学(系)研究科(研究院), 助教 (90330860)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: インフラマソーム / 神経炎症 / 痛覚過敏 / 後根神経節

Outline of Final Research Achievements

The aim of this study was to investigate the hypothesis that activation of inflammasome in the DRG contributes to the development of chronic pain hypersensitivity.
NLRP2 expression and caspase1 activity was measured in DRG of chronic inflammation model mouse. Both NLRP2 expression and caspase1 activity was increased by chronic inflammation. Caspase1 inhibitor and NLRP2 siRNA reduced pain hypersensitivity during chronic inflammation.
These results demonstrated that NLRP2 inflammasome in the DRG contributes to the development of chronic inflammatory pain hypersensitivity.

Free Research Field

疼痛治療