<i>Lactobacillus plantarum LLY-606</i> supplementation ameliorates hyperuricemia <i>via</i> modulating intestinal homeostasis and relieving inflammation

Abstract

Gut microbiota is associated with hyperuricemia progression and can be regulated by <i>Lactobacillus plantarum</i>. However, the role of <i>Lactobacillus plantarum</i> in hyperuricemia is still unknown. Thus, we constructed the mouse model of hyperuricemia using potassium oxonate and hypoxanthine treatment to explore the effects of <i>Lactobacillus plantarum LLY-606</i> supplementation on the development of hyperuricemia. The results showed that <i>Lactobacillus plantarum LLY-606</i> significantly reduced the level of serum uric acid through inhibiting uric acid secretion and regulating uric acid transport. We also found that <i>Lactobacillus plantarum LLY-606</i> supplementation inhibited the inflammatory response and the activation of the TLR4/MyD88/NF-κB signaling pathway in mice. Microbiome sequencing and analysis suggested the successful colonization of probiotics, which could regulate intestinal flora dysbiosis induced by hyperuricemia. The abundance of <i>Lactobacillus plantarum</i> was significantly negatively correlated with hyperuricemia-related indicators. Notably, the functional abundance prediction of microbiota indicated that lipopolysaccharide biosynthesis protein pathways and lipopolysaccharide biosynthesis pathways were inhibited after the probiotic intervention. In conclusion, <i>Lactobacillus plantarum LLY-606</i> can serve as a potential functional probiotic to affect the development of hyperuricemia through modulating gut microbiota, downregulating renal inflammation, and regulating uric acid metabolism.