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

Area of Science:

• Microbiology
• Immunology
• Cardiovascular Medicine

Background:

• Atherosclerosis is a major global cause of death, linked to gut dysbiosis.
• Gut microbiota disruptions promote inflammation and produce proatherogenic metabolites like trimethylamine-N-oxide (TMAO).
• Short-chain fatty acids (SCFAs) and bile acids (BAs) from gut bacteria can resolve inflammation and reduce atherogenesis.

Purpose of the Study:

• To explore the role of gut microbiota and its metabolites in atherosclerotic cardiovascular disease (ACVD).
• To investigate how gut dysbiosis influences immune processes and systemic inflammation in ACVD.
• To identify novel therapeutic strategies for ACVD targeting the gut-host-immune axis.

Main Methods:

• Review of literature on gut microbiota composition and its impact on ACVD.
• Analysis of metabolic pathways involving trimethylamine (TMA) to TMAO production.
• Examination of the anti-atherogenic effects of SCFAs and BAs.

Main Results:

• Gut dysbiosis is associated with ACVD development and chronic low-grade inflammation.
• Proatherogenic metabolites (TMAO) and beneficial metabolites (SCFAs, BAs) are produced by the gut microbiota.
• Factors like metabolic syndrome, type 2 diabetes mellitus (T2DM), and obesity are linked to chronic inflammation.

Conclusions:

• The gut microbiota plays a critical role in ACVD pathogenesis through immune modulation and metabolite production.
• Targeting gut microbiota, including SCFAs, BAs, and probiotics, offers potential therapeutic avenues for ACVD.
• Further research into the gut-host-immune system interplay is crucial for understanding and treating ACVD.