レゾルビンD2は白血球の強力な調節体であり,微生物性セプシスを制御します
Matthew Spite1, Lucy V Norling, Lisa Summers
1Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.
Nature
|October 30, 2009
まとめ
レゾルビンD2 (RvD2) は,中性粒子の移動とバクテリアの負荷を減らすことで,炎症を積極的に解消します. この脂質媒介体は,免疫解消と警戒を促すことで,敗血症モデルの生存率を高めます.
科学分野:
- 免疫学 免疫学とは
- バイオケミストリー バイオケミストリー
- 薬理学 薬理学とは
背景:
- 炎症の解消は,活発で複雑なプロセスです.
- リゾルビンは,疾患の衰退 (カタベース) を指揮する脂質媒介体です.
- 解決におけるResolvin D2 (RvD2) の特定の役割は,以前は不明でした.
研究 の 目的:
- RvD2.2の特定の解決のための機能を明らかにする.
- 過剰な炎症を軽減するRvD2のメカニズムを調査する.
- セプシスなどの炎症性疾患におけるRvD2の治療の可能性を評価する.
主な方法:
- ニュートロフィルの密輸と白血球-内皮細胞の相互作用に対するRvD2の効果を in vivoで調査した.
- Cecal ligation and puncture (CLP) によって誘発された多微生物性セプシスを持つマウスにRvD2を投与した.
- バクテリアの負荷,サイトカインの生成,免疫細胞の徴募,およびマクロファージのファゴサイトーシスに対するRvD2の影響を評価した.
主要な成果:
- RvD2は,中性粒子の炎症部位への移動を強力にステレオ選択的に減少させることが示されました.
- RvD2は,酸化窒素の産生による白血球-内皮の相互作用を低下させ,粘着受容体発現を変化させた.
- CLP誘発性セプシスでは,RvD2は細菌負荷,サイトカインレベル,中性粒子の募集を低下させ,マクロファージのファゴシトーシスを強化した.
- RvD2治療は,セプシスモデルにおける生存率を著しく増加させた.
結論:
- RvD2は,過度の炎症反応の強力な内生調節剤である.
- RvD2は複数の細胞標的を介して作用し,炎症の解消を刺激します.
- RvD2は,解消を促進しながら免疫的警戒を維持し,セプシスやその他の炎症性疾患の治療の可能性を提供します.
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