Faecal lipopolysaccharides (LPS) have attracted attention as potent elements to explain a correlation between the gut microbiota and cardiovascular disease (CVD) progression. However, the underlying mechanism of how specific gut bacteria contribute to faecal LPS levels remains unclear. We retrospectively analysed the data of 92 patients and found that the abundance of the genus Bacteroides was significantly and negatively correlated with faecal LPS levels. The controls showed a higher abundance of Bacteroides than that in the patients with CVD. The endotoxin units of the Bacteroides LPS, as determined by the limulus amoebocyte lysate (LAL) tests, were drastically lower than those of the Escherichia coli LPS; similarly, the Bacteroides LPS induced relatively low levels of pro-inflammatory cytokine production and did not induce sepsis in mice. Fermenting patient faecal samples in a single-batch fermentation system with Bacteroides probiotics led to a significant increase in the Bacteroides abundance, suggesting that the human gut microbiota could be manipulated toward decreasing the faecal LPS levels. In the clinical perspective, Bacteroides decrease faecal LPS levels because of their reduced LAL activity; therefore, increasing Bacteroides abundance might serve as a novel therapeutic approach to prevent CVD via reducing faecal LPS levels and suppressing immune responses. Increasing evidence suggests that a strong correlation exists between the gut microbiota and development of many diseases, such as coronary artery disease (CAD), heart failure (HF), obesity and related metabolic diseases, and rheumatoid arthritis 1-6. Next-generation sequencing techniques and multi-omics approaches have revealed the function of the gut microbiota and improved understanding of the mechanisms underlying disease progression 7-10. For instance, the short-chain fatty acid metabolites produced by the gut microbiota are known to play a central immune-metabolic role 11 , where trimethylamine and trimethylamine N-oxide are associated with cardiovascular disease 12. In addition, the gut microbial lipopolysaccharide (LPS) has recently attracted attention, because chronic immune cell activation is, in part, caused by the LPS-mediated stimulation of toll-like receptor 4 (TLR4) in the gu 13,14. Until now, researchers have focused on plasma LPS, and have reported that plasma LPS plays an important role in the process of activating pro-inflammatory cytokines during heart failure, and may be used to predict the development of atherosclerosis and other major advanced cardiac events 15-17. In this context,