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

被引:23
|
作者
Dutot, M. [1 ,2 ]
Grassin-Delyle, S. [3 ,4 ,5 ]
Salvator, H. [5 ,6 ]
Brollo, M. [5 ]
Rat, P. [2 ]
Fagon, R. [1 ]
Naline, E. [5 ,6 ]
Devillier, P. [5 ,6 ]
机构
[1] Yslab, F-29000 Quimper, France
[2] Univ Paris 05, Lab Chim Toxicol Analyt & Cellulaire, Sorbonne Paris Cite, CNRS,UMR 8038,Fac Pharm Paris, F-75006 Paris, France
[3] Univ Paris Saclay, Univ Versailles St Quentin, UFR Sci Sante Simone Veil, INSERM,UMR 1173, Montigny Le Bretonneux, France
[4] Univ Paris Saclay, Univ Versailles St Quentin, UFR Sci Sante Simone Veil, Plateforme Spectrometrie Masse MasSpecLab, Montigny Le Bretonneux, France
[5] Hop Foch, Dept Malad Resp, F-92150 Suresnes, France
[6] Univ Paris Saclay, Univ Versailles St Quentin En Yvelines, UFR Sci Sante Simone Veil, UPRES EA 220,Lab Pharmacol Resp, F-92150 Suresnes, France
关键词
Airway epithelial cell; fucoidan; Cytokine; SULFATED POLYSACCHARIDE; IMMUNE-RESPONSE; HUMAN NASAL; MUCIN;
D O I
10.1016/j.ijbiomac.2019.02.113
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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-1 alpha, IL-1 beta, TNF alpha, 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. (C) 2019 Elsevier B.V. All rights reserved.
引用
收藏
页码:429 / 436
页数:8
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