Different Types of Atrial Fibrillation Share Patterns of Gut Microbiota Dysbiosis

Different Types of Atrial Fibrillation Share Patterns of Gut Microbiota Dysbiosis
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不同类型的心房颤动都有肠道菌群失调的模式

DOI:
10.1128/msphere.00071-20
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发表时间:
2020-03-01
期刊:
影响因子:
4.8
通讯作者:
Yang, Xinchun
Yang, Xinchun
中科院分区:
生物学2区
文献类型:
--
作者:
Zuo, Kun;Yin, Xiandong;Yang, Xinchun

文献摘要

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已知肠道微生物群(GM)和代谢紊乱模式参与心房颤动(AF)的临床表现。然而,很少有证据表明阵发性AF(PAF)和持续性AF(psAF)中粪便微生物群的具体变化。为了提供对AF类型中GM生态失调的全面理解,我们基于宏基因组学和代谢组学分析评估了30名PAF患者、20名psAF患者和50名非AF对照的GM特征。与对照组相比,PAF和psAF患者中发现了类似的GM变化,微生物多样性增加,微生物群组成发生了类似的变化。与非AF对照组相比,PAF和psAF患者共享大部分差异分类。此外,在微生物功能和相关代谢改变方面也阐明了相似性。此外,与psAF相比,在PAF中观察到微小差异。PAF和psAF之间的一些独特的分类与某些代谢产物和心房直径相关,这可能在心房重构的发病机制中起作用。我们的研究结果表明,PAF和psAF在GM中存在许多共同特征,这些特征发生在自我终止的PAF。针对GM的预防性和治疗性措施用于早期干预以延缓AF的进展是非常必要的。
Dysbiotic gut microbiota (GM) and disordered metabolic patterns are known to be involved in the clinical expression of atrial fibrillation (AF). However, little evidence has been reported in characterizing the specific changes in fecal microbiota in paroxysmal AF (PAF) and persistent AF (psAF). To provide a comprehensive understanding of GM dysbiosis in AF types, we assessed the GM signatures of 30 PAF patients, 20 psAF patients, and 50 non-AF controls based on metagenomic and metabolomic analyses. Compared with control subjects, similar changes of GM were identified in PAF and psAF patients, with elevated microbial diversity and similar alteration in the microbiota composition. PAF and psAF patients shared the majority of differential taxa compared with non-AF controls. Moreover, the similarity was also illuminated in microbial function and associated metabolic alterations. Additionally, minor disparity was observed in PAF compared with psAF. Several distinctive taxa between PAF and psAF were correlated with certain metabolites and atrial diameter, which might play a role in the pathogenesis of atrial remodeling. Our findings characterized the presence of many common features in GM shared by PAF and psAF, which occurred at the self-terminating PAF. Preventative and therapeutic measures targeting GM for early intervention to postpone the progression of AF are highly warranted.