Introduction: There is emerging evidence linking the commensal gut microbiota with the development of cardiovascular disease and arterial thrombosis. In immunothrombosis, the host clotting system protects against the dissemination of invading microbes, not considering the huge number of microbes that interact with host physiology in a mutualistic fashion. Areas covered: Interestingly, recent research revealed that colonizing gut microbes profoundly influence host innate immune pathways that support arterial thrombus growth. The gut microbiota promotes arterial thrombus formation by enhancing the pro-adhesive capacity of the vascular endothelium, triggering hepatic von Willebrand factor synthesis and its release by Weibel-Palade body exocytosis, resulting in elevated von Willebrand factor levels and enhancing FVIII stability in plasma. Furthermore, the metabolic capacity of gut resident microbes promotes agonist-induced platelet activation and deposition. Here, we give an overview, with a focus on the vascular endothelium, on how this gut-resident microbial ecosystem contributes to arterial thrombus formation. Expert opinion: The gut microbiota and its metabolites not only act on agonist-induced platelet reactivity, but also influence the hepatic endothelial phenotype via remote signaling, facilitating arterial thrombus growth at the arterial injury site.
Keywords: Microbiota; arterial thrombosis; cardiovascular disease; endothelial cell; germ-free mouse model; immunothrombosis; platelets; toll-like receptor; trimethylamine N-oxide; von Willebrand factor.