Background: Konjac glucomannan polysaccharide (KGM), inulin oligosaccharide (inulin) and their mixture has been shown to modulate the gut-associated lymphoid tissue immunity.

Aims: The present study was mainly to determine effects of a low-level (2% w/w) KGM and inulin and their combination on dextran sodium sulfate (DSS)-induced colitis. We also determine the potential mechanisms mediating these effects of dietary fibers.

Methods: C57BL/6J mice (6 weeks of age, eight per group) were randomly assigned to consume one of the following diets: control (DSS group) or control diet supplemented with 2% (w/w) of KGM (KGM group), 2% (w/w) of inulin oligosaccharide (degree of polymerization=8)(inulin group) or KGM+Inulin (1%, w/w each (K+I group)) for 29 days, combined with the DSS drinking water (2% w/v) treatment on days 21-26. Another group served as vehicle was fed the control diet and given regular drinking water throughout the study. Fresh feces were collected on days 26-29. Mice were killed on day 30 after fasting. Segments of colon tissues were processed for histological procedure. The remaining tissues were processed to determine the gene expressions of cytokines, tight junction proteins and antioxidant enzymes.

Results: The present study indicated that DSS resulted in colonic dysplasia, severe leukocyte infiltration and enhanced gene expressions of pro-inflammatory cytokines. All fiber treatments ameliorated these indices of colitis. DSS treatment reduced the colonic gene expressions of tight junction proteins and antioxidant enzymes, which were ameliorated or normalized with fiber supplementation. In addition, all fiber treatments prevented the DSS-induced alterations in the fecal microbiota and short-chain acid levels.

Conclusion: Supplementation of low-level, 2% (w/w), of KGM polysaccharide, inulin oligosaccharide and K + I reduced the DSS-induced colitis and mucosal barrier dysfunction, which was likely to be mediated by the prebiotic effects.

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This work is licensed under a Creative Commons Attribution 4.0 License.