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-α, IL-6, IL-1β) 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.
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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-α, IL-6, IL-1β) 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.
Competing Interest Statement
The authors have declared no competing interest.
Footnotes
Author contributions. EL, SH, DOG,SOG, M involved in drafting the manuscript. EL, SH acquisition of data, data analysis. ML contributed to the conception, experimental design and interpretation of data.
Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
Funding. This work was supported by the Trinity College Dublin [Provost’s PhD Project Award 2018-2022]; Innovation Partnership Program Enterprise Ireland [IP-2023-1047-A].
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