微生物から解放された宿主糖は,腸内病原体の抗生物質後の拡大を促進します
Katharine M Ng1, Jessica A Ferreyra, Steven K Higginbottom
1Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California 94305, USA.
Nature
|September 3, 2013
まとめ
抗生物質の使用は腸内微生物群を混乱させ,サルモネッラやクロストリジウムディフィシルのような病原体が,放出された砂糖を消費することによって繁栄することを可能にします. この糖分代謝をターゲットにすることで,腸内感染症に対する新しい治療戦略が提供されます.
科学分野:
- 微生物学 微生物学とは
- 胃腸内科 胃腸内科
- 感染症 感染症は感染症です.
背景:
- 人間の腸内微生物群は,細菌の病原体から保護します.
- 微生物群の抗生物質による破壊は,腸内病原体の出現につながる可能性があります.
- 病原体が微生物群の破壊を悪用するメカニズムは,十分に理解されていません.
研究 の 目的:
- 腸内病原菌であるサルモネラ・エンテリカ・セロバール・タイフィムリウム (S. typhimurium) とクロストリジウム・ディフィシルが,抗生物質によって引き起こされる微生物群の衰えをどのように利用するのかを調査する.
- これらの病原体が腸内を拡大するために使用する共通の戦略を特定する.
主な方法:
- gnotobioticと従来のマウスでS. typhimuriumとC. difficileを研究しました.
- 炭水化物の代謝経路に欠陥のある遺伝子変異体を利用した.
- 病原体の拡大を評価するために,投与された抗生物質と外因性シアル酸.
- 粘膜の炭水化物利用度と病原体の遺伝子発現を測定した.
主要な成果:
- S. typhimuriumとC. difficileは,腸の膨張のために微生物から解放された粘膜の炭水化物 (フコゼ,シアル酸) を利用する.
- これらのカタボリック経路の遺伝的障害は,病原体の競争力を損なう.
- 抗生物質の治療は,自由シアル酸を増加させ,C. difficileとS. typhimuriumに恩恵をもたらします.
- シアリダース欠乏菌は,自由シアル酸を減少させ,C. difficileの拡大を阻害する.
結論:
- 腸内病原菌は,抗生物質による腸内炭水化物の摂取量の変化を悪用します.
- 粘膜炭水化物のカタボリズムは,病原体の拡大のための共通の戦略です.
- 病原体の炭水化物代謝をターゲットにすることは,抗生物質に関連した腸内感染症に対する潜在的な治療方法を示しています.
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