Authors
Chuan Zhang, Miaoyu Li, Tiantian Li, Xiaojie Zang, Haiyang Shi, Yaru Liu, Chengcheng Zhang, Jianxin Zhao, Qixiao Zhai, Wei Chen, Fengwei Tian
Published in
Advanced science (Weinheim, Baden-Wurttemberg, Germany). Pages e78105. Oct 06, 2026. Epub Oct 06, 2026.
Abstract
Intestinal barrier dysfunction is a pathological hallmark of ulcerative colitis (UC), yet therapeutic strategies that precisely restore epithelial integrity remain limited. Here, we identified four distinct polysaccharide fractions from Ganoderma applanatum (GAPs) and pinpointed GAP2 as the principal bioactive component that significantly ameliorates DSS-induced colitis and intestinal barrier injury. Furthermore, experiments using germ-free mice and fecal microbiota transplantation show that the barrier-repairing efficacy of GAP2 depends on the gut microbiota and their metabolic outputs. This indicates that GAP2 acts as a microbiota-directed modulator, exerting health benefits by enriching Phocaeicola vulgatus and tridecylic acid. P. vulgatus degrades GAP2 via GH16, facilitating fatty-acid metabolism to generate tridecanoic acid (absent in the mutant), which may activate the Rho/CDC42 pathway in intestinal epithelial cells to promote tight-junction assembly, thereby restoring barrier integrity. Notably, a meta-analysis of UC patient cohorts revealed that both the abundance of P. vulgatus and its capacity for tridecylic acid biosynthesis were significantly decreased. Our findings establish GAP2 as a potent postbiotic inducer that repairs the intestinal barrier via a potential P. vulgatus-tridecylic acid-Rho/CDC42 axis. This work highlights the therapeutic potential of targeting this newly identified microbe-metabolite-signaling axis for the treatment of UC and related mucosal inflammatory disorders.
PMID:
42839679
Bibliographic data and abstract were imported from PubMed on 07 Oct 2026.
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