内皮ADAM10利用定义了细菌败血症小鼠血管损伤的分子途径
Danielle N Alfano1, Mark J Miller2, Juliane Bubeck Wardenburg1
1Department of Pediatrics and.
The Journal of clinical investigation
|October 3, 2023
概括
内皮ADAM10通过调解α-毒素损伤,对黄金葡萄球菌败血症至关重要. 这种酶对于 Pseudomonas aeruginosa 和 Streptococcus pneumoniae 败血症至关重要,但对于 B 组链球菌或 Candida albicans 感染至关重要.
科学领域:
- 血管生物学 血管生物学
- 传染性疾病传染性疾病.
- 免疫学 免疫学 免疫学
背景情况:
- 内皮在败血症的发病过程中至关重要,但内皮损伤的分子机制尚不清楚.
- 血管内血栓,炎症和内皮损伤会在败血症中损害氧化.
研究的目的:
- 调查内皮ADAM10在败血症发病过程中的作用.
- 确定各种败血症病原体是否利用ADAM10依赖的通路.
主要方法:
- 使用了特定于内皮的ADAM10淘汰赛小鼠模型.
- 评估了对不同病原体的反应中的败血症致死率和微血管血栓形成.
主要成果:
- 内皮ADAM10缺陷保护小鼠免受黄金葡萄球菌,Pseudomonas aeruginosa和肺炎 estreptococcus感染.
- 在ADAM10淘汰赛中,它没有保护B组链球菌或Candida albicans败血症.
- ADAM10调解了阿尔法毒素诱导的微血管血栓形成和黄金色败血症的致死性.
结论:
- 内皮ADAM10是败血症相关的内皮损伤的关键媒介,特别是在格兰氏阴性和一些格兰氏阳性细菌感染中.
- 涉及ADAM10的病原体特异性宿主通路突出了针对性败血症疗法的潜力.
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