{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,9]],"date-time":"2026-07-09T14:15:57Z","timestamp":1783606557508,"version":"3.55.0"},"reference-count":79,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,4,15]],"date-time":"2026-04-15T00:00:00Z","timestamp":1776211200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Pharmacol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Inflammatory bowel disease (IBD) involves epithelial barrier disruption, immune dysregulation, and microbial imbalance. The present study investigated the protective mechanisms of\n                      <jats:italic>Laetiporus sulphureus<\/jats:italic>\n                      polysaccharides (LSP) in dextran sulfate sodium (DSS)-induced colitis, focusing on intestinal barrier restoration, immunomodulation, and gut microbiota remodeling.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>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\u00a0mg\/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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      LSP significantly mitigated DSS-induced colitis by reducing the disease activity index by approximately 60% (\u223c2.5-fold, p &amp;lt; 0.001) and restoring colon length (\u223c1.5-fold, p &amp;lt; 0.01). Barrier integrity improved\n                      <jats:italic>via<\/jats:italic>\n                      enhanced mucin-2 expression (\u223c3.5-fold) and tight junction proteins Occludin, Claudin-1, and ZO-1 (\u223c5\u20139-fold). LSP suppressed pro-inflammatory cytokines TNF-\u03b1, IL-6, and IL-1\u03b2 (\u223c2\u20133-fold) while upregulating anti-inflammatory mediators IL-10 and TGF-\u03b2 (\u223c2.5\u20133-fold), reflecting a rebalanced mucosal immune milieu. 16S rRNA sequencing demonstrated reversal of DSS-induced dysbiosis, characterized by a reduction in pathogenic Escherichia\u2013Shigella (\u223c3.8-fold) and Enterobacteriaceae (\u223c3.5-fold), and enrichment of beneficial taxa including\n                      <jats:italic>Lactobacillus<\/jats:italic>\n                      , Bifidobacterium, and Ruminococcus (\u223c2\u20134-fold).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>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.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fphar.2026.1705032","type":"journal-article","created":{"date-parts":[[2026,4,15]],"date-time":"2026-04-15T05:46:47Z","timestamp":1776232007000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Laetiporus sulphureus polysaccharides mitigate colitis by reshaping the gut microbiota and regulating immune responses"],"prefix":"10.3389","volume":"17","author":[{"given":"Sharafat","family":"Ali","sequence":"first","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, College of Basic Medical Science, Dalian Medical University","place":["Dalian, 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