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A previous study showed that kiwifruit polysaccharide (KFP) has benefits in relieving intestinal inflammation, while the underlying mechanism remains unresolved. The objective of this study was to investigate the regulatory effect of KFP on the gut microbiota metabolism and intestinal barrier of ulcerative colitis (UC) mice induced by dextran sulfate sodium (DSS). KFP significantly improved the UC symptoms including weight loss, shortened colon length, splenomegaly, diarrhea, hematochezia, and colon inflammation of mice. In addition, KFP could alleviate DSS-caused gut microbiota dysbiosis and increase the levels of short-chain fatty acids in the cecal contents of mice. Furthermore, the results of nontargeted and targeted metabolomics analysis combined with antibiotic treatment revealed that KFP could regulate gut microbiota-dependent tryptophan metabolism, activate the aryl hydrocarbon receptor (AhR) in colon cells, and enhance interleukin-22 production and tight junction proteins' (ZO-1, occludin, and claudin3) expression to repair the intestinal barrier in UC mice. Immunofluorescence results showed that KFP significantly upregulated the conjunction of lectin WGA and UEA1 in the UC mouse colon, implying that KFP promoted fucosylation in the colon. These results suggest that KFP alleviates UC primarily via targeting the gut microbiota involved in the AhR pathway and upregulating colon fucosylation.
Li et al. (Mon,) studied this question.