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

Abstract

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 MyD88- and TRIF-dependent signaling pathways. Aquamin, a multi-mineral supplement derived from the marine red algae Lithothamnion, is known for its anti-inflammatory properties. In this study, we demonstrate that Aquamin dose-dependently inhibits lipopolysaccharide (LPS)-induced production of pro-inflammatory cytokines (TNF-, IL-6, IL-1{beta}) and chemokines in both human peripheral blood mononuclear cells (hPBMCs) and murine bone marrow-derived macrophages (mBMDMs), without causing cytotoxicity. Mechanistic studies demonstrate that Aquamin specifically suppressed TRIF dependent IRF3 activation downstream of TLR3 and TLR4. These findings support Aquamin as a promising agent for use as an intervention in counteracting inflammatory diseases states where TLR signalling is implicated.