宿主由来の窒素は,炎症した腸内のE. coliの成長を促進する

Sebastian E Winter¹, Maria G Winter, Mariana N Xavier

¹Department of Medical Microbiology and Immunology, School of Medicine, University of California, Davis, One Shields Avenue, Davis, CA, USA.

Science (New York, N.Y.)

|February 9, 2013

まとめ

腸内の炎症は,E. coliのような特定の細菌の成長を促す分子である窒素を生成します. この宿主由来窒素は,腸の炎症中に有益な共生細菌を選択的に促進します.

科学分野:

微生物学微生物学とは
免疫学免疫学とは
胃腸内科胃腸内科

背景:

腸内炎症疾患は,微生物コミュニティの構造を変化させます.
強制性無酸素菌の減少と選択性無酸素菌Enterobacteriaceaeの増加が特徴的です.
宿主の反応と微生物の変化を結びつけるメカニズムは十分に理解されていません.

研究の目的:

ホストの炎症反応が腸内微生物コミュニティの構造をどのように形作るのかを調査する.
炎症中の細菌の成長における宿主由来分子の役割を特定する.

主な方法:

腸炎のマウスモデルを利用した.
窒素を投与し,Escherichia coliの成長に与える影響を評価した.
誘導性窒素酸化物合成酵素が不足しているマウスを検査し,窒素原産を追跡した.

主要な成果:

炎症中に発生した窒素は,大腸内のEscherichia coliに成長の利点を与えました.
誘導性酸化窒素合成酵素が欠けていたマウスは,E. coliの窒素呼吸を支えておらず,宿主由来の窒素を示した.
炎症性宿主反応は,コンメンサルEnterobacteriaceaeの成長を選択的に促進する.

結論:

炎症の副産物である宿主由来の窒素は,コンメンサルのEnterobacteriaceaeの成長を選択的に促進する.
このメカニズムには,細菌による無酸素呼吸のための電子受容体の生成が含まれています.
この相互作用を理解することは,腸内炎症疾患の管理に不可欠です.

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