外体循環中の単細胞活性化におけるC3分裂の役割
C S Rinder1, H M Rinder, K Johnson
1Department of Laboratory Medicine and Anesthesiology, Yale University School of Medicine, New Haven, CT 06520-8035, USA. christine.rinder@yale.edu
Circulation
|August 3, 1999
まとめ
早期の補完体活性化,特にC3aをブロックすると,シミュレートされた体外循環 (SECC) 中の単細胞活性化が防止されます. これは,末端補完抑制のみが血小板および中性粒子の活性化を阻害する以前の発見と対照的です.
科学分野:
- 免疫学 免疫学とは
- 心肺バイパス手術 (Cardiopulmonary Bypass) が実施されました.
- 補足システムシステムです.
背景:
- 以前の研究では,末端補完抑制 (C5a,C5b-9) が血小板および中性粒子の活性化を阻害したが,SECC中に単細胞の活性化は認められなかった.
- この研究では,C3aを阻害することによって,早期の補完体阻害が単細胞活性化を防ぐことができるかどうかを調査しました.
研究 の 目的:
- SECC中にC3aの形成を阻害することで単細胞の活性化が防止されるかどうかを判断する.
- シミュレートされた心肺バイパスにおける補完体活性化と血液細胞活性化との関係をさらに理解するために.
主な方法:
- 人間の血液と膜酸素器を用いた体外循環シミュレーション (SECC) モデル.
- C3a,C5a,C5b-9の形成を阻害するために,C3/C5コンバータゼを阻害するキメリックタンパク質であるCAB-2の投与.
- 補完体成分 (C3a,C5b-9),単細胞活性化 (CD11b),中性粒子の活性化 (CD11b,エラスタゼ),血小板活性化 (P-セレクチン,結合体) について分析する.
主要な成果:
- CAB-2は,両方の試験用量でC3aとC5b-9の形成を著しく抑制しました.
- 高用量のCAB-2は,モノサイトと中性粒子のCD11bのアップレギュレーションと中性粒子のエラスタゼ放出を著しく阻害しました.
- また,CAB-2は,血小板活性化に依存する単細胞-血小板結合体の形成を阻害した.
結論:
- 早期補完阻害 (C3a阻害) は,SECCの間に単細胞CD11bのアップレギュレーションを防止しました.
- 早期補完成分は,SECCにおける単細胞活性化に不可欠である.
- この研究は,シミュレートされた心肺バイパス中に血液細胞の活性化におけるコンプリメントシステムの役割を明らかにしています.
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