Inflammatory Response: A Crucial Way for Gut Microbes to Regulate Cardiovascular Diseases

Abstract

Gut microbiota is the largest and most complex microflora in the human body, which plays a crucial role in human health and disease. Over the past 20 years, the bidirectional communication between gut microbiota and extra-intestinal organs has been extensively studied. A better comprehension of the alternative mechanisms for physiological and pathophysiological processes could pave the way for health. Cardiovascular disease (CVD) is one of the most common diseases that seriously threatens human health. Although previous studies have shown that cardiovascular diseases, such as heart failure, hypertension, and coronary atherosclerosis, are closely related to gut microbiota, limited understanding of the complex pathogenesis leads to poor effectiveness of clinical treatment. Dysregulation of inflammation always accounts for the damaged gastrointestinal function and deranged interaction with the cardiovascular system. This review focuses on the characteristics of gut microbiota in CVD and the significance of inflammation regulation during the whole process. In addition, strategies to prevent and treat CVD through proper regulation of gut microbiota and its metabolites are also discussed.

Epigenetics of Early Cardiometabolic Disease: Mechanisms and Precision Medicine

“…The gut microbiome has been implicated in the development and progression of CVD through various poorly understood mechanisms, including modulation of host metabolism, inflammation, and immune function. [46][47][48] Bacterial epigenomics (ie, DNA methylation, posttranslational modifications of histone-like proteins, and noncoding RNA) have been shown to play critical roles in bacterial virulence, metabolism, and adaptation to the host environment in bacteria 49 ; however, until recently, a significant challenge on the progress of this research has been the lack of efficient and straightforward methods for comprehensive genomic methylome profiling in bacteria. 50 Nevertheless, there is a growing interest in gut bacterial epigenomics as a promising area of research for understanding the mechanisms underlying the gut microbiome's contribution to CVD.…”

Benefits of Biotics for Cardiovascular Diseases

“…A systematic review of human studies reported that the abundance of Faecalibacterium , Bifidobacterium , Ruminococcus and Prevotella bacteria is, in turn, associated with markers of low-grade inflammation, such as high-sensitivity C-reactive protein (hs-CRP), interleukin (IL) IL-1, IL-6, and tumor necrosis factor alpha (TNF-α). The relationships between the gut microbiota and the markers of low-grade inflammation in humans, and the benefits of a therapeutic strategy for the prevention and treatment of cardiovascular diseases, considering the gut microbiota and its relation to the innate and adaptive immune system, highlight the importance of conducting research on the human gut microbiota as a potential diagnostic tool [ 17 , 18 , 19 ].…”

The Implication of the Gut Microbiome in Heart Failure

“…The GI microbiota and the intestinal barrier have bidirectional communication and form a complex network influencing the human state of health and disease [ 14 ]. Besides its function as an organ used for digestion and absorption, the GI tract acts as an immune organ, the human body’s largest immune organ [ 25 ]. “Healthy” gut microbiota have the capacity for: preserving the stability of the intestinal wall and its barrier function; tight epithelial junctions and a normal mucosal immunity; and preventing pathogen proliferation [ 2 ].…”

“…It seems that increased levels of circulating cytokines correspond to more severe clinical symptoms and to a worse prognosis in HF patients’ survival [ 38 , 39 ]. Serum levels of TNF-alpha, IL-1 and IL-6 of HF patients are directly influenced by the amount of existing LPSs, currently thought to be leading elements of a hyperinflammatory condition [ 25 ]. While in decompensated HF patients, LPS levels appear to be directly associated with systemic inflammation markers, and they decrease following HF recompensation.…”