Enterococcus faecium Alleviates Gut Barrier Injury in C57BL/6 Mice with Dextran Sulfate Sodium-Induced Ulcerative Colitis.

Wei He,Junning Zhao,Weijie Ni,Amosy M'Koma

doi:10.1155/2021/2683465

Abstract

The involvement of gut microbiota composition in ulcerative colitis is strongly supported by previous research. Growing evidence suggests that probiotic therapy protects against inflammatory bowel disease in animal models and patients. However, as a probiotic, the role of Enterococcus faecium (E. faecium) in UC remains unclear. Nevertheless, the potential mechanism of the protective effect of E. faecium remains unknown. In this study, a dextran sulphate sodium-induced (DSS-induced) colitis model was used to detect the underlying mechanism of E. faecium in maintaining gut homeostasis. ELISA was performed to detect the levels of cytokines (TNF-α, IL-1β, IL-6, and IL-10). Furthermore, 454 pyrosequencing was used to investigate the microbiota composition in fecal samples. The results illustrate that E. faecium administration could prevent DSS-induced gut inflammation and intestinal flora imbalance. At the same time, the damage to intestinal mucosal barrier and tight junctions was partially repaired. These results demonstrate the preventive effect of E. faecium in DSS-induced intestinal injury. The present study provides new insights into the medicinal value of E. faecium for UC.

Highlights

Inflammatory bowel disease (IBD) is complex and presents many challenges to gastroenterologists [1]
Based on alcian blue staining and gut permeability, E. faecium treatment contributed to intestinal mucosal injury
The upregulation of zonula occludens-1 (ZO-1) and claudin confirmed that E. faecium was able to restore intestinal barrier function by increasing the concentration of tight junction proteins

Summary

Introduction

Inflammatory bowel disease (IBD) is complex and presents many challenges to gastroenterologists [1]. Ulcerative colitis (UC) is a major form of IBD, which is marked by aberrant inflammation within the human colon [2]. Previous studies suggest that microbiota dysbiosis and intestinal barrier dysfunction are closely related to UC [3]. Previous research has demonstrated that epithelial barrier and mucous barrier defects are strongly related to the pathogenesis of UC [5]. Suzuki indicated that the expression of occludin and zonula occludens-1 (ZO-1), which are tight junction proteins, is associated with gut permeability [6]. Recent studies have shown that microbiota could have an impact on intestinal permeability [8]

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Conclusion