A marine-sourced fucoidan solution inhibits Toll-like-receptor-3-induced cytokine release by human bronchial epithelial cells

Fucoidans are sulfated polysaccharides from brown algae, known to have immunomodulatory activity. Their effects on the response of airway epithelial cells to Toll-like receptor 3 (TLR3) stimulation have not been characterized. Our objective was to evaluate the effects of a marine-sourced fucoidan so...

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Bibliographic Details
Published in:International journal of biological macromolecules 2019-06, Vol.130, p.429-436
Main Authors: Dutot, M., Grassin-Delyle, S., Salvator, H., Brollo, M., Rat, P., Fagon, R., Naline, E., Devillier, P.
Format: Article
Language:English
Subjects:
Airway epithelial cell
Cells, Cultured
Chemical Sciences
Cytokine
Cytokines - metabolism
Dinoprostone - biosynthesis
Epithelial Cells - drug effects
Epithelial Cells - metabolism
fucoidan
Humans
Polysaccharides - pharmacology
Respiratory Mucosa - drug effects
Respiratory Mucosa - metabolism
Toll-Like Receptor 3 - metabolism
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Summary:Fucoidans are sulfated polysaccharides from brown algae, known to have immunomodulatory activity. Their effects on the response of airway epithelial cells to Toll-like receptor 3 (TLR3) stimulation have not been characterized. Our objective was to evaluate the effects of a marine-sourced fucoidan solution (MFS) on the TLR3-induced expression and/or production of cytokines and prostaglandin by human primary bronchial epithelial cells as a model of the airway epithelium. The cells were incubated with MFS in the presence or absence of Poly(I:C) (a TLR3 agonist that mimics viral RNA). Cytokine expression and production were assessed using RT-qPCR and ELISA. The expression of cyclooxygenase-2 and the production of prostaglandin E2 were also measured. Relative to control, exposure to MFS was associated with lower Poly(I:C)-induced mRNA expression of various cytokines and chemokines, and lower COX-2 production. The MFS inhibited the production of some cytokines (IL-1α, IL-1β, TNFα, and IL-6), chemokines (CCL5, CCL22, CXCL1, CXCL5 and CXCL8) and prostaglandin E2 but did not alter the production of IL-12/25, CCL2 and CCL20. At clinically relevant concentrations, the MFS inhibited the TLR3-mediated production of inflammatory mediators by human primary bronchial epithelial cells - suggesting that locally applied MFS might help to reduce airway inflammation in viral infections.
ISSN:0141-8130
1879-0003
DOI:10.1016/j.ijbiomac.2019.02.113