Saccharina japonica-Derived Fucoidan Protects Intestinal Immune Homeostasis by Modulating Dendritic Cell Function and Alleviating LPS-Induced Acute Enteritis.

Fucoidan (FUC) exhibits immunomodulatory activity; however, its effects on intestinal mucosal immunity through dendritic cell (DC)-mediated regulation remain unclear. In this study, fucoidan was extracted from Saccharina japonica by hot-water extraction and characterized by chemical composition analysis, gel permeation chromatography (GPC), and Fourier-transform infrared spectroscopy (FT-IR). Bone marrow-derived DCs were used to evaluate the effects of FUC on DC maturation and immune function. An LPS-induced acute enteritis mouse model was used to assess intestinal injury, barrier function, and DC-mediated T/B cell immune responses. Structural analysis confirmed that purified FUC has the sulfated polysaccharide characteristics. FUC promoted DC maturation and enhanced antigen-presenting capacity. In LPS-induced enteritis, FUC reduced IL-1β, IL-6, and TNF-α levels and improved intestinal barrier integrity by restoring the mRNA expression of tight-junction-related genes. Mechanistically, FUC regulated the excessive activation of the TLR4/MyD88/NF-κB pathway, increased TGF-β and IFN-γ expression, modulated Th1/Th17/Treg immune balance, and promoted B cell homing and sIgA secretion. FUC regulates DC-mediated immune responses, repairs intestinal mucosal barrier function, and restores the intestinal immune microenvironment, thereby alleviating LPS-induced intestinal inflammation and maintaining intestinal homeostasis.