Sargassum fusiforme polysaccharide activates nuclear factor kappa-B (NF-κB) and induces cytokine production via Toll-like receptors

• SFPS significantly enhanced cytokines and NO productions in peritoneal macrophages.
• Anti-TLR4 and anti-TLR2 antibody significantly blocked SFPS-induced TNF-α and NO production.
• Anti-CD14 antibody also significantly blocked SFPS-induced TNF-α and NO production.
• SFPS significantly increased the production and translocation of NF-κB to the nucleus.
• SFPS-mediated immunomodulatory activity is mediated by TLRs/NF-κB signaling pathway.

This study was designed to investigate the mechanism of macrophage activation by the Sargassum fusiforme polysaccharide (SFPS). As a result, SFPS significantly enhanced cytokines and nitric oxide (NO) productions in peritoneal macrophages, and stimulated macrophages to produce the cytokines and NO through the induction of their genes expression. The pretreatment of peritoneal macrophages with special antibodies [Toll-like receptors (TLRs) antibody] significantly blocked SFPS-induced tumor necrosis factor alpha (TNF-α) and NO production. Furthermore, pyrrolidine dithiocarbamate (PDTC), a specific inhibitor of NF-κB, effectively suppressed SFPS-induced TNF-α and interleukin 1β (IL-1β) secretion in peritoneal macrophages, indicating that SFPS stimulated macrophages to produce cytokines through the NF-κB pathway and the result was further confirmed by the experiment of Western blotting (WB) and confocal laser scanning microscope (CLSM). Taken together, these results suggest that SFPS-mediated induction of cytokines and NO production in macrophages is mediated, at least in part, by TLRs/NF-κB signaling pathway.