Aquamin, a marine derived multi-mineral, attenuates toll-like receptor-mediated inflammatory responses in macrophages.

Toll-like receptors (TLRs) play a central role in innate immune responses through recognition of pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). Activation of TLRs leads to the induction of inflammatory cytokines via myeloid differentiation primary response 88 (MyD88)- and TIR-domain-containing adaptor-inducing interferon-β (TRIF)-dependent signaling pathways. Aquamin, a multi-mineral supplement derived from the marine red algae Lithothamnion sp., is known for its anti-inflammatory properties. In this study, we demonstrate that Aquamin dose-dependently suppressed lipopolysaccharide (LPS) and Poly(I:C) production of pro-inflammatory cytokines [tumor necrosis factor-α (TNF-α) and interleukin (IL)-6] and chemokines in both human peripheral blood mononuclear cells (hPBMCs) and murine bone marrow-derived macrophages (mBMDMs), without causing cytotoxicity. The findings are consistent with Aquamin modulation of TRIF-associated signaling downstream of TLR3 and TLR4. These data provide a rationale for further investigations of Aquamin as a potential therapeutic intervention for inflammatory diseases associated with dysregulated TLR signaling.