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TREM-1放大了炎症,是败血症休克的关键调解者
A Bouchon1, F Facchetti, M A Weigand
1Basel Institute for Immunology, Grenzacherstrasse 487, CH-4005 Basel, Switzerland.
Nature
|April 27, 2001
概括
在骨髓细胞-1 (TREM-1) 上表达的触发受体增强了对细菌感染的先天免疫反应. 阻断TREM-1可以防止败血性休克,表明其治疗潜力.
科学领域:
- 免疫学 免疫学 免疫学
- 微生物学 微生物学
- 病理学 病理学 病理学
背景情况:
- 天生的免疫依赖于中性粒细胞和表达模式识别受体 (PRRs) 的单细胞/巨细胞.
- PRR刺激触发了对病原体消除和组织修复至关重要的促炎媒介.
- 在细菌感染期间过度炎症会导致组织损伤和败血症.
研究的目的:
- 调查质细胞-1 (TREM-1) 上表达的触发受体在放大对微生物产品的炎症反应中的作用.
- 评估TREM-1作为感染性休克的潜在治疗点.
主要方法:
- 在感染组织和败血症患者中对中性粒细胞和单细胞进行TREM-1表达的评估.
- 使用的小鼠模型的脂聚糖化物 (LPS) 诱导的冲击和细菌性败血症 (大肠杆菌,结和穿刺).
- 在这些模型中研究了TREM-1阻断对生存率和疾病严重程度的影响.
主要成果:
- 在中性粒细胞和透到感染组织的单细胞上,TREM-1的表达很高.
- 在患有微生物败血症的患者和小鼠冲击模型中,TREM-1在中性粒细胞上升调节.
- 阻止TREM-1显著保护小鼠免受LPS诱导的冲击和多微生物败血症.
结论:
- TREM-1在放大对细菌感染的急性炎症反应中发挥着至关重要的作用.
- TREM-1被认为是感染性休克病变的关键媒介.
- 向TREM-1代表了一种有前途的治疗策略,用于治疗败血症休克.
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