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. 2024 Jan;25(1):44-60.
doi: 10.1111/1751-2980.13249. Epub 2024 Feb 18.

Commensal Enterococcus faecalis W5 ameliorates hyperuricemia and maintains the epithelial barrier in a hyperuricemia mouse model

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Commensal Enterococcus faecalis W5 ameliorates hyperuricemia and maintains the epithelial barrier in a hyperuricemia mouse model

Xin Liu et al. J Dig Dis. 2024 Jan.

Abstract

Objective: The intestine is responsible for approximately one-third of uric acid (UA) excretion. The effect of commensal Enterococcus faecalis (E. faecalis), one of the most colonized bacteria in the gut, on UA excretion in the intestine remains to be investigated. The aim of this study was to evaluate the effect of commensal E. faecalis on UA metabolism and gut microbiota.

Methods: The 16S rRNA gene sequencing was used to examine the species of Enterococcus in mouse fecal content. E. faecalis strain was isolated from mouse feces and identified to be E. faecalis W5. The hyperuricemia (HUA) animal model was established with yeast-rich forage and 250 mg·kg-1 ·day-1 potassium oxonate. Oral administration of E. faecalis W5 was given for 20 days, serving as the Efa group.

Results: Disrupted intestinal barrier, activated proinflammatory response and low UA excretion in the intestine were found in HUA mice. After E. faecalis W5 treatment, the gut barrier was restored and serum UA level was decreased. Additionally, fecal and intestinal UA levels were elevated, intestinal urate transporter ABCG2 and purine metabolism were upregulated. Moreover, short-chain fatty acid levels were increased, and intestinal inflammation was ameliorated.

Conclusions: Commensal E. faecalis W5 ameliorated HUA through reversing the impaired gut barrier, promoting intestinal UA secretion by regulating ABCG2 expression, and decreasing intestinal UA synthesis by regulating purine metabolism. The results may provide the potential for developing treatments for HUA through the intestine.

Keywords: Enterococcus faecalis; epithelial barrier; gastrointestinal microbiome; hyperuricemia; urate transporter.

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References

REFERENCES

    1. Balakumar P, Alqahtani A, Khan NA, Mahadevan N, Dhanaraj SA. Mechanistic insights into hyperuricemia-associated renal abnormalities with special emphasis on epithelial-to-mesenchymal transition: pathologic implications and putative pharmacologic targets. Pharmacol Res. 2020;161:105209. doi:10.1016/j.phrs.2020.105209
    1. Aihemaitijiang S, Zhang YQ, Zhang L, et al. The association between purine-rich food intake and hyperuricemia: a cross-sectional study in Chinese adult residents. Nutrients. 2020;12(12):3835. doi:10.3390/nu12123835
    1. Zhao HY, Chen XY, Zhang L, et al. Lacticaseibacillus rhamnosus Fmb14 prevents purine induced hyperuricemia and alleviate renal fibrosis through gut-kidney axis. Pharmacol Res. 2022;182:106350. doi:10.1016/j.phrs.2022.106350
    1. Borghi C, Agabiti-Rosei E, Johnson RJ, et al. Hyperuricaemia and gout in cardiovascular, metabolic and kidney disease. Eur J Intern Med. 2020;80:1-11.
    1. de Oliveira EP, Burini RC. High plasma uric acid concentration: causes and consequences. Diabetol Metab Syndr. 2012;4:12. doi:10.1186/1758-5996-4-12

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