腸内微生物群とキモアトラクタント受容体GPR43による炎症反応の調節
Kendle M Maslowski1, Angelica T Vieira, Aylwin Ng
1Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst, New South Wales 2010, Australia.
Nature
|October 30, 2009
まとめ
腸内細菌によって産生される短鎖脂肪酸 (SCFA) は,炎症の解消に不可欠です. Gタンパク質結合受容体43 (GPR43) との相互作用は,正常な免疫反応と炎症性疾患の予防に不可欠です.
科学分野:
- 免疫学 免疫学とは
- 微生物学 微生物学とは
- 胃腸内科 胃腸内科
背景:
- 免疫システムは,トール型受容体 (TLR) を介して病原体を認識します.
- 腸内微生物群とその代謝産物である短鎖脂肪酸 (SCFA) は,免疫反応に影響を与え,炎症性疾患から保護する可能性があります.
- コリチス疾患は,変化した微生物群と減少したSCFAと関連しており,SCFAの摂取は臨床的な利点を示しています.
研究 の 目的:
- 炎症反応の調節におけるSCFA-Gタンパク質結合受容体43 (GPR43) 相互作用の役割を調査する.
- 様々な疾患モデルにおける炎症の解消のためのGPR43シグナル伝達の必要性を決定する.
主な方法:
- GPR43欠乏 (Gpr43(-/-)) のマウスと細菌のないマウスを利用した.
- 大腸炎,関節炎,喘息のモデルにおける炎症反応を調べた.
- 炎症媒介体の免疫細胞生産と免疫細胞の徴募を評価した.
主要な成果:
- GPR43欠乏したマウスは,大腸炎,関節炎,喘息のモデルにおいて,炎症が悪化したり,解消されない炎症を示した.
- Gpr43(-/-) 免疫細胞は,炎症媒介体の生産が増加し,免疫細胞の募集が強化されたことを示した.
- バクテリアとSCFAが欠けていた細菌のないマウスは,同様の炎症的調節障害を示した.
結論:
- SCFA-GPR43の相互作用は,炎症反応の正常な解消に不可欠である.
- GPR43シグナリングは,調節不良の炎症を予防するために不可欠であり,食事,腸内微生物群,免疫機能をリンクします.
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