微生物群の食事による調節は,自己炎症性疾患に影響する
John R Lukens1, Prajwal Gurung1, Peter Vogel2
1Department of Immunology, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.
Nature
|October 3, 2014
まとめ
ダイエット脂肪とコレステロールは,腸内微生物群を変化させ,インタールイキン-1β (IL-1β) 生産を減少させることで,マウスの炎症性骨疾患から保護します. これは,Prevotella細菌とcaspase-8シグナル伝達に関係しています.
科学分野:
- 免疫学 免疫学とは
- 微生物学 微生物学とは
- 遺伝学 遺伝学とは
- 骨の生物学 骨の生物学
背景:
- 慢性炎症性疾患は増加しており,食事も影響している可能性があるが,そのメカニズムは不明である.
- Pstpip2 ((cmo) マウスは,ヒトの慢性再発性多焦点性骨髄炎に似た骨髄炎を発症する.
- 以前の研究では,インタールイキン-1β (IL-1β) の関与が示されましたが,炎症性の成分 (カスペーゼ-1,NLRP3) はこれらのマウスを保護しませんでした.
研究 の 目的:
- Pstpip2 ((cmo)) マウスのIL-1β産生を制御するアップストリームメカニズムを特定する.
- IL-1β依存性炎症性骨の侵食を誘発する環境要因を調査する.
- 骨髄炎の病原性における食事と腸内微生物群の役割を明らかにする.
主な方法:
- Pstpip2 ((cmo)) マウスの腸内微生物群の分析.
- Pstpip2 ((cmo)) マウスにおける食事介入 (高脂肪,高コレステロールの食事)
- Pstpip2 ((cmo) と野生型のマウスの抗生物質治療と細菌のない状態.
- インフラマソームの成分 (カスパゼ-1,NLRP3) とカスパゼ (カスパゼ-1,カスパゼ-8) の遺伝的切除.
主要な成果:
- 病気のPstpip2 ((cmo) マウスは,腸内微生物群にPrevotellaの増殖を示した.
- 脂肪とコレステロールに富んだ食事は,Prevotellaとプロ-IL-1β発現を減少させ,オステオミエライトからマウスを保護しました.
- 抗生物質治療と細菌のない状態も,プロIL-1β発現を減少させた.
- カスパース-1とカスパース-8の結合デリエーションは,IL-1β依存性骨疾患に対する保護のために必要であった.
結論:
- 腸内微生物群の食事に関連した変化は,骨髄炎の重要な調節因子である.
- この発見は,Prevotella,食事,および炎症体およびカスパース-8経由によるIL-1β成熟を含む経路を強調しています.
- この研究は,食事,腸内微生物群,およびIL-1β誘発性炎症性骨疾患との新しい関連性を明らかにしています.
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