在慢性心力衰竭中,肠道失调和中性粒细胞外细胞陷在慢性心力衰竭中
Vibeke Bratseth1, Andraz Nendl2, Sajan C Raju3
1Oslo Center for Clinical Heart Research, Department of Cardiology Ullevaal, Oslo University Hospital, Oslo, Norway.
International journal of cardiology
|November 3, 2024
概括
在心力衰竭患者中,高水平的中性粒细胞外细胞陷 (NETs) 标记物素化组合素H3 (CitH3) 与疾病严重程度的增加和肠道微生物群多样性的减少有关. 这表明NET可能在渐进性心力衰竭中起作用.
科学领域:
- 心脏病学 心脏病学
- 微生物学 微生物学
- 免疫学 免疫学 免疫学
背景情况:
- 慢性心力衰竭 (HF) 与肠道微生物群多样性减少有关.
- 微生物泄漏和代谢物可能会激活中性粒细胞,导致中性粒细胞外细胞陷 (NET) 的形成.
- 由染色质和蛋白酶组成的NETs与HF病变发生有关.
研究的目的:
- 评估在HF患者中循环NET和心脏功能之间的关联.
- 研究NET与肠道微生物群多样性,肠道泄漏和微生物代谢物之间的关系.
- 探索NETs在慢性心力衰竭的严重性中的作用.
主要方法:
- 一项对124名慢性HF患者 (左心室喷射率≤40%) 的横截面研究.
- 测量NET标记物 (素基 H3 [CitH3]),肠道泄漏标记物 (脂聚糖,可溶性CD14) 和微生物代谢物 (三甲基胺N-氧化物,丁酸盐).
- 使用香农多样性指数和失生指数对肠道微生物群的表征.
主要成果:
- 升高的CitH3水平与更严重的HF显著相关.
- CitH3与高血压,较高的CRP水平和较低的肠道微生物群多样性 (香农指数) 有中度的关联.
- 没有其他NET标志物与严重的HF有显著的关联.
结论:
- 高水平的CitH3与慢性HF患者的疾病严重程度增加,炎症和肠道微生物群多样性减少有关.
- 增强的NET释放可能有助于渐进的高频.
- 肠道微生物群改变对这一过程的直接贡献似乎有限.
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