信号伝達とS. typhimuriumによる上皮細胞の侵入

J Pace¹, M J Hayman, J E Galán

¹Department of Microbiology, School of Medicine, State University of New York, Stony Brook 11794-5222.

Cell

|February 26, 1993

まとめ

Salmonella typhimuriumの侵入には,細胞内カルシウムが増加することが必要です. レウコトリエンによって媒介されるこのカルシウム増加は,細菌が宿主細胞に侵入するために不可欠です.

科学分野:

微生物学微生物学とは
細胞生物学細胞生物学
パトジェネシス (病原生)

背景:

ホスト細胞の侵入は,サルモネラ菌の病原性にとって極めて重要です.
Salmonella typhimuriumの侵入は,上皮細胞の表皮成長因子受容体を活性化させます.

研究の目的:

Salmonella typhimuriumの侵入における細胞内カルシウムの役割を調査する.
細菌が宿主細胞に侵入する際の分子メカニズムを特定する.

主な方法:

S. typhimurium感染時に表皮細胞の細胞内カルシウム濃度を測定する.
侵襲性欠陥変異体とカルシウム抗体を使用しています.
レウコトリエンとフォスフォリファーゼA2の活性への影響を評価する.
ミトゲン活性化タンパク質キナーゼ活性化のモニタリング.

主要な成果:

S. typhimuriumの侵入は,細胞内カルシウム ([Ca2+]i) の急速な増加を引き起こします.
侵襲性欠陥変異体はカルシウム流入を誘発できず,カルシウム対抗剤は野生型の侵入を抑制しました.
レウコトリエンの生成につながるフォスフォリファーゼA2と5-リポキシゲナーゼの活動は,侵入のために必要である.
レウコトリエンD4は[Ca2+]iの増加を誘発し,侵入障害のある変異体の内部化を引き起こした.
S. typhimuriumの感染により,ミトゲン活性化タンパク質キナーゼが活性化されました.

結論:

細胞内カルシウムの増加は,サルモネラ型ヒモリウムの宿主細胞への侵入の前提条件である.
レウコトリエンの生成は,細菌の侵入に必要なカルシウム流入を媒介するために不可欠です.
この研究は,サルモネラ宿主細胞の侵入に関与する重要なシグナル伝達経路を明らかにしています.

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