E-カデリンは,L. monocytogenesが上皮細胞に侵入するために必要な表面タンパク質であるインターナリンの受容体です
J Mengaud1, H Ohayon, P Gounon
1Unité des Interactions Bactéries-Cellules, Station Centrale de Microscopie Electronique, Institut Pasteur, Paris, France.
Cell
|March 22, 1996
まとめ
研究者らは,E-cadherinを,Listeria monocytogenesのタンパク質であるインターナリンの細胞受容体として特定しました. この相互作用は,非ファゴサイト細胞へのバクテリアの侵入を媒介し,宿主-病原菌の相互作用のための新しいメカニズムを明らかにします.
科学分野:
- 微生物学 微生物学とは
- 細胞生物学 細胞生物学
- 分子生物学は分子生物学である.
背景:
- Listeria monocytogenesのようなグラム陽性細菌は,宿主細胞を侵略することができます.
- 細菌が非胞細胞に侵入する特定の細胞受容体とメカニズムは完全に理解されていません.
- インターナリンは,L. monocytogenesの侵入に不可欠な主要な毒性因子です.
研究 の 目的:
- L. monocytogenesの宿主細胞への侵入に不可欠なタンパク質であるインターナリンの細胞受容体を特定する.
- L.monocytogenesが非胞細胞に侵入するメカニズムを解明する.
主な方法:
- アフィニティクロマトグラフィーは,internalin.のリガンドを特定するために使用されました.
- 機能的測定は,鶏のE-カデリンの同型体 (L-CAM) で線維細胞を移植し,細菌の侵入を測定することを含む.
- 抗体阻害実験は,受容体の特異性を確認するために行われました.
主要な成果:
- E-カデリンは,内定の細胞受容体として特定されました.
- 線維芽細胞におけるL-CAMの発現は,L. monocytogenesのエントリーを著しく強化した.
- また,L-CAM発現は,内部リンリンを発現するリコンビネントのL. innocua株の侵入を促した.
- L-CAMを標的とした抗体は,内部リン媒介の細菌の侵入を阻害した.
- リステリア菌の侵入は,サルモネラ菌の侵入とは異なり,膜のラッフリングなしに誘発されたファゴサイトーシスによって起こります.
結論:
- E-カデリンは,L.monocytogenesが内部リンタンパク質経由で非ファゴサイト細胞に侵入することを媒介する細胞受容体です.
- この相互作用は,バクテリアの侵入の新たなメカニズムと,E-cadherinのための新しいタイプの異性愛相互作用を表しています.
- この経路を理解することで,宿主-病原体相互作用と潜在的な治療標的の洞察が得られます.
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