Fengwei Tian

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.

BL-99 improved FC symptoms in the short term and may benefit gut health by modulating the gut microbiota and related pathways.

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Dysregulation of the microbiota–gut–brain axis has been implicated in Parkinson’s disease (PD), and modulation of the intestinal microbiota may offer a complementary nutritional approach. This study evaluated the preventive attenuation of MPTP-induced PD-like abnormalities by Lactiplantibacillus plantarum SHOU LAC-1 and examined associated microbiota–gut–brain axis-related changes. Forty male C57BL/6J mice were allocated to Control, MPTP, L-DOPA, and SHOU LAC-1 groups (n = 10 per group). SHOU LAC-1 was orally administered at 1 × 10⁹ CFU per mouse per day for 42 days, with MPTP administered during the final 14 days; L-DOPA was administered during the MPTP-treatment period as a positive control. Motor performance and defecatory parameters, nigrostriatal TH and α-SYN immunoreactivity, neurotrophic-support-related gene expression, inflammatory markers, glial-cell-related gene expression, Nrf2-related antioxidant gene expression, colonic histopathology and tight-junction-related gene expression, gut microbiota composition, and serum metabolic profiles were assessed. Compared with MPTP-treated mice, SHOU LAC-1-treated mice showed better motor and defecatory performance, partial preservation of nigrostriatal TH immunoreactivity, reduced α-SYN immunoreactivity, increased neurotrophic-support-related gene expression, lower central and colonic inflammatory markers and glial-cell-related gene expression, increased Nrf2/HO-1/NQO1-related antioxidant gene expression, and comparatively better-preserved colonic morphology with higher tight-junction-related gene expression. 16S rRNA sequencing and untargeted serum metabolomics further showed that SHOU LAC-1 administration was accompanied by changes in gut microbial diversity and composition and serum metabolic profiles. Overall, under this preventive experimental design, SHOU LAC-1 administration was associated with attenuation of multiple MPTP-induced PD-like abnormalities, accompanied by changes in gut microbial and serum metabolic profiles. These preclinical findings are predominantly associative; causal relationships among microbial, metabolic, intestinal, and neurological changes remain to be established, and the translational relevance of SHOU LAC-1 requires further validation.