心梗可导致肠道菌群移位
Title：
Gut-dependent microbial translocation induces inflammation and cardiovascular events after ST-elevation myocardial infarction
Abstract：
Post-infarction cardiovascular remodeling and heart failure are the leading cause of myocardial infarction (MI)-driven death during the past decades. Experimental observations have involved intestinal microbiota in the susceptibility to MI in mice; however, in humans, identifying whether translocation of gut bacteria to systemic circulation contributes to cardiovascular events post-MI remains a major challenge.Here, we carried out a metagenomic analysis to characterize the systemic bacteria in a cohort of 49 healthy control individuals, 50 stable coronary heart disease (CHD) subjects, and 100 ST-segment elevation myocardial infarction (STEMI) patients. We report for the first time higher microbial richness and diversity in the systemic microbiome of STEMI patients. More than 12% of post-STEMI blood bacteria were dominated by intestinal microbiota (Lactobacillus, Bacteroides, and Streptococcus). The significantly increased product of gut bacterial translocation (LPS and d-lactate) was correlated with systemic inflammation and predicted adverse cardiovascular events. Following experimental MI, compromised left ventricle (LV) function and intestinal hypoperfusion drove gut permeability elevation through tight junction protein suppression and intestinal mucosal injury. Upon abrogation of gut bacterial translocation by antibiotic treatment, both systemic inflammation and cardiomyocyte injury in MI mice were alleviated.Our results provide the first evidence that cardiovascular outcomes post-MI are driven by intestinal microbiota translocation into systemic circulation. New therapeutic strategies targeting to protect the gut barrier and eliminate gut bacteria translocation may reduce or even prevent cardiovascular events post-MI.
All Authors：
Xin Zhou, Jing Li, Junli Guo, Bin Geng, Wenjie Ji, Qian Zhao, Jinlong Li, Xinlin Liu, Junxiang Liu,Zhaozeng Guo, Wei Cai, Yongqiang Ma, Dong Ren , Jun Miao , Shaobo Chen , Zhuoli Zhang , Junru Chen7 ,Jiuchang Zhong, Wenbin Liu , Minghui Zou , Yuming Li， Jun Cai
First Authors：
Xin Zhou, Jing Li, Junli Guo
Correspondence：
Yuming Li， Jun Cai
摘要：
对49名健康对照、50名稳定性冠心病和100名ST段抬高心肌梗死（STEMI）患者的血液菌群进行分析发现： STEMI后，患者的血液菌群丰度和多样性升高，且超过12%的血液细菌来自肠道菌群；血液中肠道菌群产物显著增加，与STEMI后的系统性炎症和不良心血管事件相关；另外， 心肌梗死小鼠模型中，左心室功能减退和肠灌注不足，使紧密连接蛋白表达下降、肠粘膜受损，导致肠道通透性升高；经过抗生素治疗消除肠道细菌移位，可缓解模型小鼠的系统性炎症与心肌细胞损伤。