アピコンプレックス寄生虫は宿主カルパインをコオプトし,感染した細胞から脱出するのを容易にします

Rajesh Chandramohanadas¹, Paul H Davis, Daniel P Beiting

¹Department of Pharmacology, University of Pennsylvania, Philadelphia, PA 19104, USA.

Science (New York, N.Y.)

|April 4, 2009

まとめ

プラズモジアやトキソプラズマのような寄生虫原生体は,宿主のカルパインタンパク質を駆使して逃げる. カルパインを阻害すると,寄生虫の脱出を阻止し,それを回復すると寄生虫が宿主細胞から出ることができる.

科学分野:

細胞生物学細胞生物学
寄生虫学とは,寄生虫学である.
分子生物学は分子生物学である.

背景:

アピコンプレックス寄生虫は,世界的な疾病負担を大きく引き起こす.
これらの原生動物は細胞内での複製を行い,拡散するためには脱出しなければなりません.

研究の目的:

宿主細胞のカルパインプロテアゼがアピコンプレックス寄生虫の脱出に果たす役割を調査する.
カルパインがPlasmodium falciparumとToxoplasma gondiiにとって不可欠であるかどうかを判断するには,出口.

主な方法:

免疫低下,薬理学的阻害,RNA干渉,遺伝的消去を活用した.
細胞生物学的および遺伝的補完アプローチを採用した.
赤い細胞からPlasmodium falciparumと,線維芽細胞からToxoplasma gondiiの脱出を研究した.

主要な成果:

カルパイン-1の抑制または減少は,プラズモディウム・ファルシパラムの赤血球からの排出を阻害しました.
浄化されたカルパイン-1. 1を添加するとエグレスが回復しました.
トキソプラズマ・ゴンディの脱出は,カルパイン抑制または消去によって抑制された.
遺伝的補完は,両方の寄生虫モデルでエグレスを復元しました.

結論:

ホスト細胞のカルパインプロテアゼは,アピコンプレックス寄生虫の脱出に不可欠です.
カルパインをターゲットにすることは,寄生虫の伝播を抑制する潜在的な戦略です.

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