The role of mitochondrial function on the on the surgical stress induced immune suppression.

2018 Fiscal Year Final Research Report

• Project/Area Number: 16K10978
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Anesthesiology
• Research Institution: University of Occupational and Environmental Health, Japan
• Principal Investigator: KAWASAKI TAKASHI 産業医科大学, 医学部, 教授 (60299633)
• Co-Investigator(Kenkyū-buntansha): 川崎 知佳 産業医科大学, 医学部, 非常勤医師 (60258621)
• Project Period (FY): 2016-04-01 – 2019-03-31
• Keywords: 外科的侵襲 / 免疫能 / ミトコンドリア / 白血球

Outline of Final Research Achievements

The purpose of this study was to investigate the role of mitochondrial function on the surgical stress induced immune suppression. Neutrophils (PMN-Ⅱ) appears in association with surgical injury play a role on the increased susceptibility of patients to various infections and were known to produce IL-10 and CCL2. The production of IL-12 and CCL3 by blood from trauma-hemorrhage mice was suppressed compared to control mice. The blood from surgical mice confirmed as PMN-Ⅱrich blood, because these blood produced IL-10, but not IL-12 and CCL3. CoQ10 treatment improved IL-12 and CCL3 production. Oligomycin treatment further suppressed IL-12 production and increased IL-10 and CCL2 production. These results indicate that mitochondrial function plays a role in maintain immune function and CoQ10 may be a beneficial treatment for surgical injured patients.

Free Research Field

麻酔科学

Academic Significance and Societal Importance of the Research Achievements

本研究により、外科侵襲下の免疫担当細胞のプロフィール変化とミトコンドリア機能障害とのinteractionについて検討することができた。また、ミトコンドリア機能障害を抑制し白血球のプロフィール変化を制御することで、SSI発生、周術期感染性合併症発生を抑える戦略を開発できる可能性がある。ハイリスク、コンプロマイズドホストの症例増加が予想される将来にも貢献できるものと考える。