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在心肌梗塞后的中性粒细胞衍生S100A8/A9放大粒细胞形成

Gopalkrishna Sreejit^1,2, Ahmed Abdel-Latif³, Baskaran Athmanathan^1,2

¹Department of Surgery (G.S., B.A., P.R.N.), Ohio State University Wexner Medical Center, Columbus.

|January 17, 2020

概括

心肌梗塞 (MI) 通过S100A8/A9激发中性粒细胞的产生. 破坏这种途径可以改善心脏功能,并可能减少心血管不良事件.

科学领域:

心血管生物学
免疫学
血液形成

背景情况:

心肌梗塞 (MI) 增加了中性粒细胞的产生,但根本的机制尚未完全理解.
在心脏病发作后持续的中性粒细胞产生和招募对于心脏修复和炎症至关重要.
了解这些机制是开发针对心脏病患者的治疗方法的关键.

研究的目的:

阐明驱动MI诱导的骨髓形成和中性粒细胞扩张的分子机制.
研究特定的警示素和信号通路在MI后炎症中的作用.
探索针对中性粒细胞相关途径的治疗策略,以改善心脏结果.

主要方法:

使用老鼠模型进行永久左前下垂动脉绑定研究.
采用流细胞测量来表征髓状细胞群.
对心脏细胞进行全球转录组分析,并使用遗传/药物干预.
通过心声学评估心脏功能,并分析患者的临床相关性.

主要成果:

诱导S100A8/A9警示蛋白的快速中性细胞招募和释放.
激活托尔类受体4和NLRP3炎症体,促进互白素-1β的分泌.
介质素-1β刺激了造血干细胞中的颗粒形成,增加了中性粒细胞的产生.
在小鼠中阻断S100A8/A9或下游通路抑制了颗粒形成并改善了心脏功能.
在急性冠状动脉综合征患者中,中性粒细胞数量升高与不良结果相关.

结论:

中性细胞衍生的S100A8/A9警示素是心肌损伤后的炎症反应的核心.
针对S100A8/A9信号传递或下游介质 (NLRP3,IL-1β) 是一种潜在的治疗策略.
通过这些途径抑制颗粒形成可以改善急性冠状动脉综合征的心脏功能.

关键词:

S100A8/A9,Nlrp3炎症体警示剂发生炎症骨髓形成心肌缺血症中性粒细胞

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