Gut Dysbiosis and Immune System in Atherosclerotic Cardiovascular Disease (ACVD)

Atherosclerosis is a leading cause of cardiovascular disease and mortality worldwide. Alterations in the gut microbiota composition, known as gut dysbiosis, have been shown to contribute to atherosclerotic cardiovascular disease (ACVD) development through several pathways. Disruptions in gut homeostasis are associated with activation of immune processes and systemic inflammation. The gut microbiota produces several metabolic products, such as trimethylamine (TMA), which is used to produce the proatherogenic metabolite trimethylamine-N-oxide (TMAO). Short-chain fatty acids (SCFAs), including acetate, butyrate, and propionate, and certain bile acids (BAs) produced by the gut microbiota lead to inflammation resolution and decrease atherogenesis. Chronic low-grade inflammation is associated with common risk factors for atherosclerosis, including metabolic syndrome, type 2 diabetes mellitus (T2DM), and obesity. Novel strategies for reducing ACVD include the use of nutraceuticals such as resveratrol, modification of glucagon-like peptide 1 (GLP-1) levels, supplementation with probiotics, and administration of prebiotic SCFAs and BAs. Investigation into the relationship between the gut microbiota, and its metabolites, and the host immune system could reveal promising insights into ACVD development, prognostic factors, and treatments.

Automated summary

Atherosclerosis, a major cause of cardiovascular disease, can be influenced by alterations in the gut microbiota composition, leading to gut dysbiosis. This dysbiosis activates immune processes and systemic inflammation, contributing to the development of atherosclerotic cardiovascular disease (ACVD). The gut microbiota produces metabolites, such as trimethylamine (TMA) and short-chain fatty acids (SCFAs), that can either promote or decrease atherogenesis. Understanding the relationship between the gut microbiota and the host immune system could provide insights into ACVD development, prognostic factors, and potential treatments.