Fu Zhi-Ping, Lee Shuang, Wang Rui-Yao, Wang Yu-Qing
Collage of Pharmacology, North China University of Science and Technology, Tangshan 063200, China.
iScience. 2024 Jul 25;27(9):110572. doi: 10.1016/j.isci.2024.110572. eCollection 2024 Sep 20.
Sepsis-induced arrhythmia, linked to sudden cardiac death, is associated with gut microbiota, though the exact relationship is unclear. This study aimed to elucidate the relationship between () and arrhythmia. The relative abundance of was increased in cecal ligation and puncture (CLP)-induced septic mice. Live , supernatant, and outer membrane vesicles (OMVs) resulted in premature ventricular beat (PVB), sinus arrhythmia (SA), and increased arrhythmia and mortality in sepsis model through dysregulated ion channel proteins. Moreover, short-chain fatty acids (SCFAs) showed antibacterial effects . We confirmed sodium acetate (C2) and sodium butyrate (C4) protect from -induced arrhythmia, and C2 and C4 protected from septic arrhythmia by activating free fatty acid receptor 2 and 3 (FFAR2 and FFAR3) in mice. These findings point to how 's OMVs trigger arrhythmia, and SCFAs may be a treatment for septic arrhythmia.
脓毒症诱导的心律失常与心源性猝死有关,它与肠道微生物群有关,尽管确切关系尚不清楚。本研究旨在阐明()与心律失常之间的关系。在盲肠结扎和穿刺(CLP)诱导的脓毒症小鼠中,()的相对丰度增加。活的()、上清液和外膜囊泡(OMV)通过离子通道蛋白失调导致脓毒症模型中出现室性早搏(PVB)、窦性心律失常(SA),并增加心律失常和死亡率。此外,短链脂肪酸(SCFA)显示出抗菌作用。我们证实醋酸钠(C2)和丁酸钠(C4)可预防()诱导的心律失常,并且C2和C4通过激活小鼠中的游离脂肪酸受体2和3(FFAR2和FFAR3)预防脓毒症性心律失常。这些发现指出了()的OMV如何引发心律失常,并且SCFA可能是治疗脓毒症性心律失常的一种方法。