フラビウイルスによる全身感染後の腸動不全症候群
James P White1, Shanshan Xiong2, Nicole P Malvin2
1Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Cell
|October 9, 2018
まとめ
腸内ニューロンを標的とするウイルス感染は,マウスの急性損傷と慢性腸内不運動を引き起こす可能性があります. 免疫細胞はこれらの運動障害において重要な役割を果たし,新しい診断と治療戦略を示唆しています.
科学分野:
- 神経科学
- 免疫学
- 胃腸内科
背景:
- 慢性胃腸不運動症候群は 世界中で流行していますが 原因は不明です
- 腸内神経系感染症は腸の運動障害に 関わっている.
研究 の 目的:
- 腸内神経細胞におけるフラビウイルス感染の役割とその胃腸障害への寄与を調査する.
- フラビウイルスに起因する腸機能不全における 免疫反応,特に CD8+ T細胞を調査する.
主な方法:
- 胃腸系における急性および慢性効果を研究するためにマウスをフラビウイルスに感染させた.
- CD8+T細胞の役割を 遺伝子削除と養子移植実験で調べました
- 関連のないウイルスワクチンと炎症刺激による慢性運動障害の悪化を調べた.
主要な成果:
- フラビウイルス感染は急性損傷,炎症,マウスの腸経路の遅延を引き起こした.
- フラビウイルスに誘発されたCD8+T細胞は,神経損傷と運動遅延において決定的であった.
- 感染後のマウスは慢性的な胃腸不運動を発症し,二次刺激により悪化した.
結論:
- 腸内ニューロンを標的とするウイルスの感染は慢性的な胃腸不運動を引き起こします.
- 免疫反応,特にCD8+T細胞は,これらの疾患の重要な媒介です.
- このマウスモデルは,ヒトの感染後の腸の運動障害と潜在的な治療目標についての洞察を提供します.
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