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髄膜球菌性毒ショックにおける心筋機能不全におけるインタールイキン6の役割
Nazima Pathan1, Cheryl A Hemingway, Ash A Alizadeh
1Department of Paediatrics, Imperial College of Science, Technology and Medicine, W2 1PG, London, UK. n.pathan@imperial.ac.uk
Lancet (London, England)
|January 24, 2004
まとめ
インタールイウキン6 (IL-6) は,髄膜球菌性性ショックにおける心筋縮を引き起こす. この炎症性サイトカインは,心臓機能不全と疾患の重症度の重要な要因であり,潜在的な治療目標を提供します.
科学分野:
- 心臓病学 心臓病学
- 免疫学 免疫学とは
- 感染症 感染症とは
背景:
- 心筋不全はセプティックショックにおいて極めて重要であり,臓器の損傷や死亡につながる.
- セプシスは,心臓の収縮性を損なう要因の放出を誘発します.
- 髄膜炎球菌性 сепティックショックにおけるこれらの心筋緩剤の特定は極めて重要です.
研究 の 目的:
- 髄膜球菌性 септик шокにおける心筋縮の特定のメディエーターを特定する.
- セプシス誘発の心臓機能不全における血清因子の役割を調査する.
主な方法:
- 遺伝子発現プロファイリング,タンパク質,細胞分析を組み合わせた.
- メンニゴコックスの暴露後の血液中のアップレギュレーション遺伝子を特定しました.
- 選択された熱安定タンパク質 (12-25 kDa) を潜在的心筋抑うつ因子として用いる.
主要な成果:
- 174のアップレギュレーション遺伝子を特定し,6つのコード化されたタンパク質が,心筋抑うつ因子の特性と一致しました.
- インタールイキン6 (IL-6) は,インビトロにおいて,ミオカルディアの有意な低下を誘発した.
- IL-6の除去により,患者の血清と細胞のスーパーナタンにおけるネガティブなイノトロピック活性が廃止された.
- 血清のIL-6レベルは,小児における心筋機能不全と疾患の重症度と相関する.
結論:
- インターリューキン6は,髄膜球菌疾患における心筋縮の重要な媒介体である.
- IL-6とその下流経路は,髄膜炎球菌性結核ショックの潜在的な治療標的を代表しています.
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