Fucoidan from Costaria costata alleviated dextran sulfate sodium-induced ulcerative colitis by suppressing dendritic cell activation.

Abstract

Fucoidan, a water-soluble polysaccharide commonly derived from seaweed, is known for its diverse biological activities. Fucoidan from Costaria costata (FCC) suppresses lipopolysaccharide (LPS)-induced sepsis and lung inflammation by inhibiting dendritic cell (DC) activation. In this study, we investigated the anti-inflammatory effect of FCC in a mouse model of ulcerative colitis (UC), which is a chronic inflammatory disease of the colon. Orally administered FCC significantly inhibited UC severity induced by dextran sulfate sodium (DSS) intake. In particular, FCC administration decreased the infiltration of T cells and neutrophils into the colon of DSS-treated mice. Furthermore, FCC suppressed the DSS-induced production of interferon-gamma (IFN-γ) and interleukin 17 (IL-17) in colonic T cells. However, FCC did not directly suppress IFN-γ and IL-17 production in CD4 T cells. FCC administration also reduced the DSS-induced increase in the number of DCs in mesenteric lymph node (mLN). Additionally, FCC suppressed DSS-induced upregulation of co-stimulators and major histocompatibility complex (MHC) molecules in mLN DCs. FCC also inhibited LPS-induced DC activation, which resulted in reduced T cell proliferation and differentiation. These findings demonstrate that oral FCC alleviates UC by targeting DCs and T cell activity, thereby highlighting its potential as a therapeutic agent for intestinal inflammation.