Xin Liu, Chun Hua Han, Tao Mao, Jie Wu, Le Yong Ke, Ying Jie Guo, Rong Shuang Han, Zi Bin Tian
{"title":"共生粪肠球菌 W5 可改善高尿酸血症并维持高尿酸血症小鼠模型的上皮屏障","authors":"Xin Liu, Chun Hua Han, Tao Mao, Jie Wu, Le Yong Ke, Ying Jie Guo, Rong Shuang Han, Zi Bin Tian","doi":"10.1111/1751-2980.13249","DOIUrl":null,"url":null,"abstract":"<div>\n \n <section>\n \n <h3> Objective</h3>\n \n <p>The intestine is responsible for approximately one-third of uric acid (UA) excretion. The effect of commensal <i>Enterococcus faecalis</i> (<i>E. faecalis</i>), 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 <i>E. faecalis</i> on UA metabolism and gut microbiota.</p>\n </section>\n \n <section>\n \n <h3> Methods</h3>\n \n <p>The 16S rRNA gene sequencing was used to examine the species of <i>Enterococcus</i> in mouse fecal content. <i>E. faecalis</i> strain was isolated from mouse feces and identified to be <i>E. faecalis</i> W5. The hyperuricemia (HUA) animal model was established with yeast-rich forage and 250 mg·kg<sup>−1</sup>·day<sup>−1</sup> potassium oxonate. Oral administration of <i>E. faecalis</i> W5 was given for 20 days, serving as the Efa group.</p>\n </section>\n \n <section>\n \n <h3> Results</h3>\n \n <p>Disrupted intestinal barrier, activated proinflammatory response and low UA excretion in the intestine were found in HUA mice. After <i>E. faecalis</i> 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.</p>\n </section>\n \n <section>\n \n <h3> Conclusions</h3>\n \n <p>Commensal <i>E. faecalis</i> 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.</p>\n </section>\n </div>","PeriodicalId":15564,"journal":{"name":"Journal of Digestive Diseases","volume":"25 1","pages":"44-60"},"PeriodicalIF":2.3000,"publicationDate":"2023-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Commensal Enterococcus faecalis W5 ameliorates hyperuricemia and maintains the epithelial barrier in a hyperuricemia mouse model\",\"authors\":\"Xin Liu, Chun Hua Han, Tao Mao, Jie Wu, Le Yong Ke, Ying Jie Guo, Rong Shuang Han, Zi Bin Tian\",\"doi\":\"10.1111/1751-2980.13249\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>\\n \\n <section>\\n \\n <h3> Objective</h3>\\n \\n <p>The intestine is responsible for approximately one-third of uric acid (UA) excretion. The effect of commensal <i>Enterococcus faecalis</i> (<i>E. faecalis</i>), 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 <i>E. faecalis</i> on UA metabolism and gut microbiota.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Methods</h3>\\n \\n <p>The 16S rRNA gene sequencing was used to examine the species of <i>Enterococcus</i> in mouse fecal content. <i>E. faecalis</i> strain was isolated from mouse feces and identified to be <i>E. faecalis</i> W5. The hyperuricemia (HUA) animal model was established with yeast-rich forage and 250 mg·kg<sup>−1</sup>·day<sup>−1</sup> potassium oxonate. Oral administration of <i>E. faecalis</i> W5 was given for 20 days, serving as the Efa group.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Results</h3>\\n \\n <p>Disrupted intestinal barrier, activated proinflammatory response and low UA excretion in the intestine were found in HUA mice. After <i>E. faecalis</i> 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.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Conclusions</h3>\\n \\n <p>Commensal <i>E. faecalis</i> 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.</p>\\n </section>\\n </div>\",\"PeriodicalId\":15564,\"journal\":{\"name\":\"Journal of Digestive Diseases\",\"volume\":\"25 1\",\"pages\":\"44-60\"},\"PeriodicalIF\":2.3000,\"publicationDate\":\"2023-12-21\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Digestive Diseases\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1111/1751-2980.13249\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"GASTROENTEROLOGY & HEPATOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Digestive Diseases","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/1751-2980.13249","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"GASTROENTEROLOGY & HEPATOLOGY","Score":null,"Total":0}
Commensal Enterococcus faecalis W5 ameliorates hyperuricemia and maintains the epithelial barrier in a hyperuricemia mouse model
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.
期刊介绍:
The Journal of Digestive Diseases is the official English-language journal of the Chinese Society of Gastroenterology. The journal is published twelve times per year and includes peer-reviewed original papers, review articles and commentaries concerned with research relating to the esophagus, stomach, small intestine, colon, liver, biliary tract and pancreas.