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在对自由胆固醇和胆固醇残留物的反应中,人类巨细胞的亲炎性两极分化

Paukner Karel^1,2, Muffova Barbora^1,2, Bartuskova Hana¹

¹Laboratory for Atherosclerosis Research, Centre for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic.

Physiological reports

|May 23, 2025

概括

巨细胞中自由胆固醇 (FC) 的升高与前炎性反应和动脉样硬化发展相关. 这项研究将FC积累与巨细胞激活联系起来,表明这种慢性炎症疾病的关键机制.

科学领域:

心血管生物学心血管生物学
免疫学免疫学免疫学
代谢性疾病代谢性疾病

背景情况:

动脉样硬化是一种由脂蛋白驱动的慢性炎症性血管疾病.
巨细胞激活是动脉样硬化的主要原因,自由胆固醇 (FC) 参与了它们的炎症状态.
将巨细胞中的FC积累与炎症联系在一起的机制尚未完全理解.

研究的目的:

研究人类受试者脂蛋白水平,巨细胞表型和FC积累之间的相关性.
阐明FC积累对巨细胞炎症基因表达和表面受体配置文件的体外影响.

主要方法:

在56名健康个体中,对巨标记物 (CD14+,CD16+,CD36high,CD163+) 与脂质样本 (LDL-C,残留颗粒,HDL-C) 的相关性分析.
在体外研究中,将巨细胞暴露在FC中,以评估基因表达 (TNF-α,CCL3,ACAT,CD36) 和表面受体变化 (CD206,CD16).

主要成果:

在促炎性巨细胞 (CD14+CD16+CD36高) 和LDL-C/残留颗粒之间发现了正相关性.
抗炎性巨细胞 (CD14+CD16-CD163+) 与HDL-C呈负相关性.
在体外,FC积累的巨细胞上调了TNF-α和CCL3,改变了CD206和CD16的表达,并增加了颗粒度.

结论:

巨细胞中过度的自由胆固醇积累促进了亲炎性反应,导致动脉样硬化.
巨细胞的FC积累改变了表面受体表达,并增强了细胞颗粒度.
研究结果表明,FC积累,全身炎症和动脉样硬化病原体之间存在联系.

关键词:

脂肪组织的脂肪组织.动脉样硬化动脉样硬化胆固醇/细胞和组织这是一种炎症炎症炎症炎症.脂蛋白质是一种脂蛋白质.

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