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2023 Fiscal Year Final Research Report

Towards therapeutic application of neutrophil-secreted extracellular vesicles in sepsis

Research Project

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Project/Area Number 19K07562
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 49050:Bacteriology-related
Research InstitutionJuntendo University

Principal Investigator

Kumagai Yumi  順天堂大学, 医学部, 助教 (90277591)

Co-Investigator(Kenkyū-buntansha) 射場 敏明  順天堂大学, 医学部, 教授 (40193635)
長岡 功  順天堂大学, 大学院医学研究科, 教授 (60164399)
Project Period (FY) 2019-04-01 – 2024-03-31
Keywords敗血症 / 細胞外小胞 / 好中球 / LL-37 / 抗菌作用 / シグナル伝達経路 / レポーターマウス
Outline of Final Research Achievements

The research representative showed that the human host defense peptide LL-37 enhances in releasing extracellular vesicles (EVs) from neutrophils. The EV possesses antimicrobial and anti-inflammatory functions, effectively acting in a mouse sepsis model. Furthermore, lactoferrin and CAMP contained in EVs were implicated in antimicrobial activity, and the Ca2+-calpain-ROCK pathway was identified as contributing to LL-37-mediated EV generation. When a Ca2+ ionophore was applied to neutrophils along with LL-37, EV generation was enhanced, leading to improved antimicrobial activity. Currently, a system utilizing knock-in reporter mice is being constructed to identify the physiological target cells of EVs.

Free Research Field

細胞外小胞

Academic Significance and Societal Importance of the Research Achievements

敗血症は細菌感染が主因となっておこるが、未だに有効な治療法は存在せず、先進国でも患者の25-60%が死亡するという致死率の高い重篤な疾患である。研究代表者がすでに示している、好中球由来の細胞外小胞 (Extracellular Vesicles, EV) が敗血症モデルマウスの病態を改善するという事実に加えて、本研究では、EVに含まれる抗菌活性分子や、EV生成に関わるシグナル伝達経路を明らかにした。またEVの標的細胞の同定を現在試みているが、これらの研究結果はすべて、EVを利用した敗血症の有効な治療法を開発するための貴重な情報であると考えられる。

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Published: 2025-01-30  

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