サルモネラ病原性の島は,ファゴサイトNADPH酸化酵素の2依存逃避である
A Vazquez-Torres1, Y Xu, J Jones-Carson
1Department of Medicine, University of Colorado Health Sciences Center, Denver, CO 80262, USA.
Science (New York, N.Y.)
|March 4, 2000
まとめ
サルモネラ・タイフィムリウム (Salmonella typhimurium) は,そのSPI2分泌システムを用いて,マクロファージを殺すのを回避する. NADPH酸化酵素を阻害すると,細菌の生存が回復し,SPI2が免疫細胞防衛機構に干渉することを示す.
科学分野:
- 微生物学 微生物学とは
- 免疫学 免疫学とは
- バクテリア病原菌の発生
背景:
- サルモネラ病原性島2 (SPI2) 型III分泌系は,サルモネラウイルスの毒性およびマクロファージ内の細胞内生存に不可欠である.
- マクロファージは,NADPH酸化酵素に依存した呼吸器爆発のようなメカニズムを使用して,細胞内病原体を排除します.
研究 の 目的:
- サルモネラ・タイフィムリウムがマクロファージ媒介による殺戮を回避する過程におけるSPI2の役割を調査する.
- マクロファージの感染中にSPI2がNADPH酸化酵素システムに干渉するかどうかを判断する.
主な方法:
- 機能的なSPI2と機能のないサルモネラ・タイフィムリウム菌株を使用する2.
- バクテリアの生存率を評価するためにマクロファージ感染モデルを使用する.
- マクロファージにおけるNADPH酸化酵素の活性を操作する.
- 超構造的および免疫光顕微鏡を用いて,NADPH酸化酵素の局所化を視覚化します.
主要な成果:
- SPI2は,サルモネラ・タイフィムリウムに,マクロファージのNADPH酸化酵素による殺戮に抵抗することを可能にします.
- NADPH酸化酵素呼吸器爆発の廃止は,マクロファージ内のSPI2変異細菌の生存を回復し,マウスのウイルス性を回復しました.
- 顕微鏡検査により,SPI2型変異細菌を含む真空の近くに位置するNADPH酸化酵素が検出されたが,野生型細菌は検出されなかった.
結論:
- SPI2分泌システムは,サルモネラ菌が宿主の先天的な免疫防御,特にNADPH酸化酵素に対抗する能力の重要な要因です.
- SPI2は,NADPH酸化酵素を含む小胞の正常な輸送をファゴソームに妨害することで機能し,それによって病原体の破壊を防ぐ可能性が高い.
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