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TREM-1は炎症を増幅し,セプティックショックの重要な媒介者である
A Bouchon1, F Facchetti, M A Weigand
1Basel Institute for Immunology, Grenzacherstrasse 487, CH-4005 Basel, Switzerland.
Nature
|April 27, 2001
まとめ
ミエロイド細胞-1 (TREM-1) に発現するトリガリング受容体は,細菌感染に対する先天的な免疫反応を強化する. TREM-1を阻害すると,セプティックショックから保護され,治療の可能性が示されます.
科学分野:
- 免疫学 免疫学とは
- 微生物学 微生物学とは
- 病理学 パトロジー
背景:
- 生まれつきの免疫は,ニュートロフィールおよびパターン認識受容体 (PRR) を発現するモノサイト/マクロファージに依存しています.
- PRRの刺激は,病原体除去と組織修復に不可欠な炎症促進媒介体を誘発する.
- バクテリア感染時の過度の炎症は,組織損傷と сепティックショックを引き起こす可能性があります.
研究 の 目的:
- マイロイド細胞-1 (TREM-1) に発現するトリガリング受容体が,微生物製品に対する炎症反応を強める役割について調査する.
- セプティックショックにおける潜在的な治療標的としてTREM-1を評価する.
主な方法:
- 感染した組織と敗血症患者の中性粒子のおよび単細胞のTREM-1発現を評価した.
- リポポリサッカリド (LPS) 誘発性ショックと細菌性セプシス (E. coli,ケカル・リガーションとパンクチャー) のマウスモデルを使用した.
- これらのモデルでTREM-1ブロックが生存率と疾患の重症度に与える影響を調査した.
主要な成果:
- TREM-1は,感染した組織に浸透する中性子細胞と単細胞に高度に発現します.
- TREM-1は,微生物性敗血症の患者およびショックのマウスモデルにおける中性粒子の上位調節されます.
- TREM-1を阻害することで,LPS誘発のショックと多微生物性セプシスに対して,マウスは著しく保護された.
結論:
- TREM-1は,細菌感染症に対する急性炎症反応の増幅に重要な役割を果たします.
- TREM-1は, септикショックの病原性における重要な媒介者として関与しています.
- TREM-1をターゲットにすることは, септикショックを管理するための有望な治療戦略を表しています.
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