| Project/Area Number |
16K10079
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pediatrics
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| Research Institution | Nippon Medical School |
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Principal Investigator |
Ohashi Ryuji 日本医科大学, 医学部, 大学院教授 (00328783)
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| Co-Investigator(Kenkyū-buntansha) |
深澤 隆治 日本医科大学, 医学部, 准教授 (80277566)
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| Project Period (FY) |
2016-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2019: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2018: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 川崎病 / 血管炎 / マクロファージ / 動脈硬化 / 免疫応答 / エクソソーム / miRNA / 病理学 |
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| Outline of Final Research Achievements |
To explore mechanisms in development of vascular lesions in Kawasaki Disease (KD), a role of exosomal micro RNA (miRNA) and phenotypes of macrophages into vascular walls were investigated. Although exosome levels appeared to be increased in serum of mouse models with arteritis, we were unable to achieve the conclusive results on roles of exosomal miRNA in human KD due to the limited number of samples and technical difficulties. In assessment of macrophage phenotypes in histological sections of the coronary arteries from human KD, the proportion of M1 phenotype, detected by CD86 or SOCS3, was higher in KD than in adult patients with atherosclerosis. In contrast, the proportion of M2, detected by CD163 or MRC1, was higher in atherosclerosis. We conclude that despite histological similarities between KD and atherosclerosis, these two diseases have a different immunological etiology for progression of the chronic vascular lesions.
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| Academic Significance and Societal Importance of the Research Achievements |
川崎病は、乳幼児に見られる原因不明の全身性血管炎である。合併症として急性期の冠動脈炎が知られているが、成人後も動脈瘤、動脈硬化などの後遺症を残す。今回、川崎病慢性期の冠動脈血管壁内に浸潤した炎症細胞に含まれるマクロファージの形質(M1/M2 macrophage)を成人の動脈硬化病変と比較したところ、成人の動脈硬化ではM2が優位であったのに対し、川崎病ではM1が優位であった。この結果は、川崎病慢性期の血管病変の進展機序が、成人動脈硬化とは異なることを示唆している。今後、川崎病血管病変の発症機序解明への道が拓けると思われる。
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