deficiency regulates gut microbiota, decreases systemic inflammation, and alleviates atherosclerosis.

Altered composition of the gut microbiota affects immunity and metabolism. This study previously found that gene knockdown changes the composition of the intestinal flora in the gene knockdown mouse model. is significantly increased in the model. This study was designed to investigate the role of in the pathogenesis of atherosclerosis. Transcriptomic data from 117 patients with coronary artery disease (CAD) and 79 healthy individuals were obtained. and / mice on normal chow diet or a high-fat diet were treated for 16 weeks; deficiency was evaluated atherosclerosis. mice on normal chow diet or a high-fat diet were treated with by daily oral gavage for 16 weeks. Moreover, one group was treated with lipopolysaccharide at 12 weeks. The levels of , , and were notably higher in the patients with CAD than in the healthy individuals. deficiency altered the composition of gut microbiota. deficiency reduced the atherosclerotic lesion formation in / mice compared with the mice. The microbial sequencing and metabolomics analysis demonstrated some beneficial bacterial (, , and ) and metabolic levels significantly had deference in / mice compared with the mice. Correlational studies indicated that had close correlations with low-density lipoprotein cholesterol, lesion area, and necrotic area. inhibited high-fat diet-induced inflammation and atherosclerotic lesion, increasing the expression of tight junction proteins (ZO-1 and claudin-1) and reducing the gut permeability. However, lipopolysaccharide reversed the protective effect of against atherosclerosis. deficiency protected against atherosclerosis by regulating the composition of gut microbiota and metabolites. attenuated atherosclerotic lesions by reducing inflammation and increasing gut permeability.IMPORTANCE deficiency modulates the gut microbiota and multiple metabolites in atherosclerotic mice. was reduced in the gut of atherosclerotic mice, but administration of reversed intestinal barrier dysfunction and vascular inflammation. Our findings suggest that targeting individual species is a beneficial therapeutic strategy to prevent inflammation and atherosclerosis.