AIMS: W) and clarify the underlying mechanism involving the gut microbiota and its metabolites. MATERIALS AND METHODS: W to evaluate atherosclerotic plaque development and stability. Gut microbiota composition and short-chain fatty acid levels were analyzed. Antibiotic-induced microbiota depletion and fecal microbiota transplantation (FMT) were used to verify the mediating role of the gut microbiota. In vitro assays were performed to examine the effects of propionate on macrophage inflammation and polarization. KEY FINDINGS: W notably increased propionate levels in cecal contents and serum. Propionate directly suppressed inflammatory responses and M1 macrophage polarization in vitro. SIGNIFICANCE: W as a promising and safe intervention for atherosclerosis and provide new mechanistic insights into the crosstalk between gut microbial metabolites and vascular inflammation.
Meng et al. (Thu,) studied this question.