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KAKEN_15K09459seika.pdf
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:Nov 12, 2018 |
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炎症性疾患におけるImmunothrombosisの制御異常と新たな治療法の開発
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エンショウセイ シッカン ニ オケル Immunothrombosis ノ セイギョ イジョウ ト アラタナ チリョウホウ ノ カイハツ
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Enshōsei shikkan ni okeru Immunothrombosis no seigyo ijō to aratana chiryōhō no kaihatsu
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Investigation of dysregulated immunothrombosis in inflammatory diseases and development of a new therapeutic tool.
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平橋, 淳一
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ヒラハシ, ジュンイチ
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Hirahashi, Junichi
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慶應義塾大学・医学部(信濃町)・講師
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Research team head
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科研費研究者番号 : 70296573
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2018
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科学研究費補助金研究成果報告書
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2017
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| Abstract |
ヒストンは損傷した宿主細胞から放出され, 炎症に伴う血栓症を惹起する。血小板の活性化はヒストン誘発性血栓症の原因であるが, 好中球依存性メカニズムは未知である。好中球除去およびMac-1欠損は, ヒストンによる肺血栓塞栓症の発症を抑制しマウスの生存を延長した。我々は血漿の存在下で血小板・好中球相互作用によって誘導される血漿凝固産物を推定する濁度測定技術を利用した。ヒストンは, 好中球Mac-1を直接活性化しMac-1依存的に血漿凝塊の産生を増大させ血小板・好中球複合体形成を増強した。これらのデータは, ヒストンが好中球-血小板相互作用を介してMac-1依存性の血栓塞栓症を誘導することを示している。
Histones are released from damaged host cells and act as mediators of inflammation-related thrombosis. Platelet activation and aggregation is responsible for histone-induced thrombosis, but neutrophil-dependent mechanisms are still unclear. Immunodepletion of neutrophils and genetic ablation of Mac-1 protected mice from histone-induced pulmonary thromboembolism and prolonged survival. We utilized turbidimetric technic which estimates plasma clot production induced by interaction between human platelets and neutrophils in the presence of plasma in vitro. Histones augmented the plasma clot production in Mac-1-dependent manner and enhanced platelet-neutrophil complex formation which is inhibited by anti-Mac-1 antibody.
Furthermore histones could directly activate Mac-1 besides through platelets . In conclusion, histones induces Mac-1-dependent thromboembolism through neutrophil-platelet interaction, which is a new therapeutic target for inflammation-induced thrombosis.
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研究種目 : 基盤研究(C)(一般)
研究期間 : 2015～2017
課題番号 : 15K09459
研究分野 : 炎症と血栓
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