Research Article: The changes of gut microbiota after acute myocardial infarction in rats

Date Published: July 7, 2017

Publisher: Public Library of Science

Author(s): Ze-Xuan Wu, Su-Fang Li, Hong Chen, Jun-Xian Song, Yuan-Feng Gao, Feng Zhang, Cheng-Fu Cao, Sunil K. Ahuja.

http://doi.org/10.1371/journal.pone.0180717

Abstract

Recent studies suggested that gut microbiota was involved in the development of coronary artery disease. However, the changes of gut microbiota following acute myocardial infarction (AMI) remain unknown. In this study, a total of 66 male Wistar rats were randomly divided into control, AMI and SHAM groups. The controls (n = 6) were sacrificed after anesthesia. The AMI model was built by ligation of left anterior descending coronary artery. The rats of AMI and SHAM groups were sacrificed at 12 h, 1 d, 3 d, 7 d and 14 d post-operation respectively. Gut microbiota was analyzed by 16S rDNA high throughput sequencing. The gut barrier injuries were evaluated through histopathology, transmission electron microscope and immunohistochemical staining. The richness of gut microbiota was significantly higher in AMI group than SHAM group at 7 d after AMI (P<0.05). Principal coordinate analysis with unweighted UniFrac distances revealed microbial differences between AMI and SHAM groups at 7 d. The gut barrier impairment was also the most significant at 7 d post-AMI. We further identified the differences of microorganisms between AMI and SHAM group at 7 d. The abundance of Synergistetes phylum, Spirochaetes phylum, Lachnospiraceae family, Syntrophomonadaceae family and Tissierella Soehngenia genus was higher in AMI group compared with SHAM group at 7 d post-operation (q<0.05). Our study showed the changes of gut microbiota at day 7 post AMI which was paralleled with intestinal barrier impairment. We also identified the microbial organisms that contribute most.

Partial Text

The role of gut microbiota in regulation of health and disease has been attracting increasing attention recently. The human gastrointestinal tract is estimated to contain approximately 100 trillion bacterial cells, belonging to 1,000 bacterial species.[1] The genome of all these microorganisms contains 100 times more genes than the human genome.[2] Recent studies showed that gut microbiota is involved in the development of coronary artery disease (CAD) through several mechanisms. Firstly, increase absorption of energy from gut may contribute to obesity and metabolic disturbances which in turn contribute to cardiovascular risk. This effect is partly mediated by short chain fatty acids (SCFAs), in particular butyrate, which are end-products of microbial fermentation of dietary fibers and play an important role in the energy harvest from the gut and maintaining the integrity of the gut barrier.[3, 4] The other mechanism involves the production of the proatherosclerotic metabolite, trimethylamine-N-oxide (TMAO). The metabolism of dietary phosphatidylcholine and L-carnitine by intestinal microbiota, results in the formation of the metabolite trimethylamine and further conversion to TMAO. TMAO was associated with atherosclerosis and elevated plasma levels of TMAO predict an increased risk of cardiovascular disease including incidence myocardial infarction.[5–8]

Previous studies have demonstrated that gut microbiota is linked to coronary artery disease. However, when and how the microbial communities alter post-AMI remains unclear. In this study, we observed the changes of gut microbiota and gut barrier post-AMI in a rat model. We found that the gut microbiota were significantly changed as early as 7 d post-AMI, paralleled with gut barrier impairment. The richness of gut microbiota was significantly higher in AMI group than SHAM group at 7 d after AMI. We also identified the microorganisms that significantly changed at 7 d after AMI.

Our study showed the changes of gut microbiota at day 7 post AMI which was paralleled with intestinal barrier impairment. We also identified the microbial organisms that were significantly altered. Our study provides the experimental basis for the study on the relationship between the AMI and intestinal flora.

 

Source:

http://doi.org/10.1371/journal.pone.0180717

 

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