Microorganism–Immune Interactions in the Pathophysiology of Cardiovascular Diseases

Cardiovascular diseases (CVDs) remain the leading cause of death worldwide and are now increasingly recognized as conditions with a strong immunoinflammatory component. Beyond traditional risk factors, microorganisms—including bacteria, viruses, and the commensal microbiota—shape cardiovascular outcomes through their interplay with innate and adaptive immune pathways. Gut microbiome-derived metabolites such as trimethylamine-N-oxide (TMAO) and the translocation of microbial products like lipopolysaccharide (LPS) into the circulation drive low-grade inflammation, endothelial activation, and immune cell reprogramming. Pattern-recognition receptors, especially Toll-like receptors (TLRs), link microbial signals to vascular inflammation, atherogenesis, and myocardial injury, while excessive production of reactive oxygen species (ROS) and activation of cell death pathways further amplify tissue damage.This Research Topic focuses on how host–microorganism interactions regulate innate and adaptive immune responses in the pathophysiology of CVDs. We welcome experimental, clinical, and translational studies that dissect cellular signaling pathways, immunometabolic changes, and epigenetic and microRNA-mediated mechanisms triggered by microbial infection or dysbiosis. Particular interest is given to work on metabolic endotoxemia, periodontal and cardiotropic pathogens, biofilm-associated infections such as infective endocarditis, and the impact of antimicrobial resistance on immune control of cardiovascular infections. Studies addressing immunomodulatory or microbiome-targeted strategies that restore immune homeostasis and mitigate cardiovascular inflammation are especially encouragedWe welcome articles addressing, but not limited to, the following themes:-Innate immune sensing of microbial products (e.g., LPS, peptidoglycan, viral RNA/DNA) by Toll-like receptors (TLRs) and other pattern-recognition receptors in vascular and cardiac tissues-Crosstalk between innate and adaptive immune responses in microbe-associated atherogenesis, plaque progression, and plaque instability-Impact of gut microbiome composition and metabolites (e.g., TMAO, short-chain fatty acids) on systemic inflammation, immunometabolism, and cardiovascular risk-Role of metabolic endotoxemia and microbial translocation in promoting endothelial dysfunction, leukocyte recruitment, and chronic low-grade vascular inflammation-Contribution of periodontal and other extra-intestinal infections to systemic immune activation, endothelial injury, and cardiovascular events-Modulation of microRNAs, epigenetic marks, and gene expression in immune and cardiovascular cells in response to microbial infection or dysbiosis-Mechanisms of ROS generation, oxidative stress, and infection-induced activation of apoptotic and other cell death pathways in cardiomyocytes and vascular cells-Immune responses to bacterial biofilms on heart valves and intracardiac devices, including immune evasion, persistence, and complications of infective endocarditis-Influence of cardiotropic viruses and other pathogens on intracellular signaling pathways (e.g., NF-κB, MAPK) that govern inflammatory, antiviral, and tissue-remodeling responses in the heart-Impact of antimicrobial resistance on host–pathogen dynamics, immune control of cardiovascular infections, and outcomes of immunomodulatory or microbiome-targeted therapies Topic editors: Amal D Premarathna, Carolina Nunes França Source: https://www.frontiersin.org/research-topics/80169/microorganism-immune-interactions-in-the-pathophysiology-of-cardiovascular-diseases