Frontiers in pharmacology · 2026
Laetiporus sulphureus polysaccharides mitigate colitis by reshaping the gut microbiota and regulating immune responses.
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Ali Sharafat, Alioui Yamina, Khan Imran, Ullah Hidayat, Rahman Mujeeb Ur, Atta Aamna, Abusidu Mohammed, Ilyas Muhammad, Noor Uzma, Ma Renzhen, Ali Muhsin, Farooqui Nabeel Ahmed, Deng Ting, Wang Guangyang, Xin Yi, Sha Shanshan, Ma Yufang
Аннотация
BACKGROUND: Inflammatory bowel disease (IBD) involves epithelial barrier disruption, immune dysregulation, and microbial imbalance. The present study investigated the protective mechanisms of Laetiporus sulphureus polysaccharides (LSP) in dextran sulfate sodium (DSS)-induced colitis, focusing on intestinal barrier restoration, immunomodulation, and gut microbiota remodeling.
METHODS: LSP was structurally characterized using HPLC, FTIR, and SEM analyses, revealing a heteropolysaccharide primarily composed of glucose (55.16%), galactose (16.55%), and mannose (13.52%). Experimental colitis was induced in BALB/c mice with 3% DSS, followed by oral LSP administration (200 or 400 mg/kg). Disease severity, histopathology, barrier markers, cytokine profiles, macrophage polarization, and gut microbiota composition were evaluated using biochemical assays, immunofluorescence, IHC, and 16S rRNA sequencing.
RESULTS: LSP significantly mitigated DSS-induced colitis by reducing the disease activity index by approximately 60% (∼2.5-fold, p < 0.001) and restoring colon length (∼1.5-fold, p < 0.01). Barrier integrity improved via enhanced mucin-2 expression (∼3.5-fold) and tight junction proteins Occludin, Claudin-1, and ZO-1 (∼5-9-fold). LSP suppressed pro-inflammatory cytokines TNF-α, IL-6, and IL-1β (∼2-3-fold) while upregulating anti-inflammatory mediators IL-10 and TGF-β (∼2.5-3-fold), reflecting a rebalanced mucosal immune milieu. 16S rRNA sequencing demonstrated reversal of DSS-induced dysbiosis, characterized by a reduction in pathogenic Escherichia-Shigella (∼3.8-fold) and Enterobacteriaceae (∼3.5-fold), and enrichment of beneficial taxa including Lactobacillus, Bifidobacterium, and Ruminococcus (∼2-4-fold).
CONCLUSION: LSP exerts multi-targeted protection against colitis by reinforcing epithelial barrier function, attenuating inflammation, and reshaping gut microbial ecology. These findings highlight LSP as a promising natural therapeutic candidate for IBD. Further metabolomic and meta transcriptomic analyses are warranted to elucidate the microbial metabolites and molecular pathways mediating these protective effects.
METHODS: LSP was structurally characterized using HPLC, FTIR, and SEM analyses, revealing a heteropolysaccharide primarily composed of glucose (55.16%), galactose (16.55%), and mannose (13.52%). Experimental colitis was induced in BALB/c mice with 3% DSS, followed by oral LSP administration (200 or 400 mg/kg). Disease severity, histopathology, barrier markers, cytokine profiles, macrophage polarization, and gut microbiota composition were evaluated using biochemical assays, immunofluorescence, IHC, and 16S rRNA sequencing.
RESULTS: LSP significantly mitigated DSS-induced colitis by reducing the disease activity index by approximately 60% (∼2.5-fold, p < 0.001) and restoring colon length (∼1.5-fold, p < 0.01). Barrier integrity improved via enhanced mucin-2 expression (∼3.5-fold) and tight junction proteins Occludin, Claudin-1, and ZO-1 (∼5-9-fold). LSP suppressed pro-inflammatory cytokines TNF-α, IL-6, and IL-1β (∼2-3-fold) while upregulating anti-inflammatory mediators IL-10 and TGF-β (∼2.5-3-fold), reflecting a rebalanced mucosal immune milieu. 16S rRNA sequencing demonstrated reversal of DSS-induced dysbiosis, characterized by a reduction in pathogenic Escherichia-Shigella (∼3.8-fold) and Enterobacteriaceae (∼3.5-fold), and enrichment of beneficial taxa including Lactobacillus, Bifidobacterium, and Ruminococcus (∼2-4-fold).
CONCLUSION: LSP exerts multi-targeted protection against colitis by reinforcing epithelial barrier function, attenuating inflammation, and reshaping gut microbial ecology. These findings highlight LSP as a promising natural therapeutic candidate for IBD. Further metabolomic and meta transcriptomic analyses are warranted to elucidate the microbial metabolites and molecular pathways mediating these protective effects.