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Published on: July 26, 2017
Aquamin, a marine derived multi-mineral, attenuates toll-like receptor-mediated inflammatory responses in macrophages
Emmanouil Lioudakis1, Sakshi Hans1, Denise M O'Gorman2
1Department of Pharmacology and Therapeutics, School of Medicine, Trinity College Dublin, Dublin, Ireland.
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 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.
Insights
Aquamin, a marine algae supplement, reduces inflammatory cytokine production by modulating Toll-like receptor (TLR) signaling pathways. This suggests Aquamin
Area of Science:
- Immunology
- Pharmacology
- Marine Biotechnology
Background:
- Toll-like receptors (TLRs) are key in innate immunity, recognizing pathogen- and damage-associated molecular patterns.
- TLR activation triggers inflammatory cytokine release via MyD88- and TRIF-dependent pathways.
- Aquamin, derived from marine algae, exhibits known anti-inflammatory effects.
Purpose of the Study:
- To investigate Aquamin's impact on TLR-mediated inflammatory responses.
- To elucidate the signaling pathways involved in Aquamin's anti-inflammatory action.
Main Methods:
- Human peripheral blood mononuclear cells (hPBMCs) and murine bone marrow-derived macrophages (mBMDMs) were treated with Aquamin.
- Cells were stimulated with lipopolysaccharide (LPS) or Poly(I:C) to activate TLRs.
- Pro-inflammatory cytokine and chemokine production was measured.
- Cytotoxicity was assessed.
Main Results:
- Aquamin dose-dependently suppressed TNF-α and IL-6 production induced by LPS and Poly(I:C).
- Aquamin did not exhibit cytotoxicity in tested cell types.
- The anti-inflammatory effects align with modulation of TRIF-associated signaling downstream of TLR3 and TLR4.
Conclusions:
- Aquamin effectively suppresses TLR-induced pro-inflammatory cytokine and chemokine production.
- Aquamin's mechanism involves modulating TRIF-dependent TLR signaling.
- Aquamin shows potential as a therapeutic agent for inflammatory diseases linked to TLR dysregulation.
