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Murine Colitis Modeling using Dextran Sulfate Sodium DSS
Published on: January 19, 2010
Xylo-oligosaccharide supplementation exacerbates colitis susceptibility in mice via taurine depletion
Yiwen Li1, Haocun Kong2, Caiming Li1
1State Key Laboratory of Food Science and Resources, Jiangnan University, Wuxi 214122, China; School of Food Science and Technology, Jiangnan University, Wuxi 214122, China; Institute of Future Food Technology, JITRI, Yixing 214200, China.
Abstract:
Xylo-oligosaccharides (XOS) are widely utilized as functional food ingredients and additives. However, the impact of long-term dietary supplementation with XOS on intestinal inflammation and its underlying mechanisms has yet to be fully elucidated. This study investigated the XOS supplementation on susceptibility to DSS-induced ulcerative colitis (UC) in C57BL/6 J mice and explored the underlying mechanisms, with a particular focus on the intestinal microenvironment and bile acids (BAs) metabolism. The experimental results demonstrated that a 12-week dietary intervention with XOS markedly aggravated UC in mice. In contrast, short-term supplementation with XOS during the induction period of UC did not lead to a further increase in disease severity. Microbiota analysis revealed that long-term dietary supplementation with XOS reduced gut microbial diversity and altered the composition, notably decreasing Ileibacterium and Family_XIII_AD3011_group while enriching Bifidobacterium. Furthermore, XOS disrupted BAs metabolism, with significant reductions in taurine (TAU) and taurocholic acid levels. To confirm the relevance of these metabolic alterations, TAU was supplemented following 12 weeks of dietary XOS intake. TAU supplementation markedly alleviated UC symptoms, improved histopathological outcomes, and promoted epithelial regeneration by upregulating genes such as Olfm4 and Clu, while restoring total and specific bile acids with known epithelial-protective functions. These findings underscore that while XOS has promising prebiotic properties, prolonged supplementation may disrupt intestinal homeostasis and exacerbate UC.

