Format

Send to

Choose Destination
Microbiome. 2018 Apr 3;6(1):66. doi: 10.1186/s40168-018-0441-4.

Gut-dependent microbial translocation induces inflammation and cardiovascular events after ST-elevation myocardial infarction.

Author information

1
Tianjin Key Laboratory of Cardiovascular Remodeling and Target Organ Injury, Pingjin Hospital Heart Center, 220, Cheng-Lin Street, Tianjin, 300162, China.
2
Heart Center, Beijing Chao Yang Hospital, Capital Medical University, Beijing, 100020, China.
3
Beijing Key Laboratory of Hypertension, Beijing, 100020, China.
4
Cardiovascular Institute of Affiliated Hospital, Hainan Medical College, Haikou, 571199, China.
5
Hypertension Center, Fuwai Hospital, State Key Laboratory of Cardiovascular Disease of China, National Center for Cardiovascular Diseases of China, Chinese Academy of Medical Sciences and Peking Union Medical College, Xicheng District, North Lishi Road No. 167, Beijing, 100037, China.
6
Department of Radiology, Northwestern University, Chicago, IL, 60611, USA.
7
Novogene Bioinformatics Institute, Beijing, 100000, China.
8
Eminent Scholar in Molecular Medicine, Georgia Research Alliance, Georgia State University, Atlanta, USA.
9
Tianjin Key Laboratory of Cardiovascular Remodeling and Target Organ Injury, Pingjin Hospital Heart Center, 220, Cheng-Lin Street, Tianjin, 300162, China. cardiolab@gmail.com.
10
Hypertension Center, Fuwai Hospital, State Key Laboratory of Cardiovascular Disease of China, National Center for Cardiovascular Diseases of China, Chinese Academy of Medical Sciences and Peking Union Medical College, Xicheng District, North Lishi Road No. 167, Beijing, 100037, China. caijun@fuwaihospital.org.

Abstract

BACKGROUND:

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.

RESULTS:

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.

CONCLUSIONS:

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.

KEYWORDS:

Cardiovascular outcome; Gut permeability; Microbial translocation; Myocardial infarction

PMID:
29615110
PMCID:
PMC5883284
DOI:
10.1186/s40168-018-0441-4
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for BioMed Central Icon for PubMed Central
Loading ...
Support Center