Commensal Enterococcus faecalisW5 Ameliorates Hyperuricemia and Maintains the Epithelium Barrier in a Hyperuricemia Mouse Model

Abstract

AbstractObjectiveThe intestine plays an important role in uric acid (UA) metabolism, accounting for one‐third of urate excretion. Commensal Enterococcus faecalis (E. faecalis), one of most colonized bacteria in the gut, yet is little known about its effect on the excretion of UA in the intestine. The purpose of this research was to examine the effect of commensal E. faecalis on the intestine and the development of hyperuricemia.Methods16s RNA gene sequencing was used to examine the species of Enterococcus in mouse fecal content. Isolated and cultured an E. faecalis strain from mouse feces and identified the strains was E. faecalis W5. A hyperuricemia (HUA) animal model was established with yeast‐rich forage and 250 mg. kg−1. d−1 potassium oxonate, followed by oral administration of E. faecalis W5 for 20 days.ResultsDysbiosis intestinal barrier, activating the pro‐inflammatory response and low UA excretion in the intestine were found in HUA mice. While the gut barrier was repaired and the serum UA level was decreased after E. faecalis W5 treatment. The fecal and intestinal UA level was elevated, and the intestinal urate transporter ABCG2 was upregulated. As well as the was regulated. Moreover, the short chain fatty acids were increased, and inflammation was ameliorated.ConclusionThese results demonstrated that the commensal E. faecalis W5 ameliorated hyperuricemia through by reversing impaired barrier, promoting intestinal UA secretion by regulating ABCG2 expression, and decreasing intestinal UA synthesis by regulating purine metabolism. The results may offer potential for developing hyperuricemia therapeutic strategies through the intestine.This article is protected by copyright. All rights reserved.