Short fungal fractions of beta-1,3 glucans ...
Type de document :
Article dans une revue scientifique
PMID :
URL permanente :
Titre :
Short fungal fractions of beta-1,3 glucans affect platelet activation
Auteur(s) :
Vancraeyneste, Helene [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Charlet, Rogatien [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Guerardel, Yann [Auteur]
Unité de Glycobiologie Structurale et Fonctionnelle UMR 8576 [UGSF]
Choteau, Laura [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Bauters, Anne [Auteur]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Tardivel, Meryem [Auteur]
Université de Lille, Droit et Santé
Francois, Nadine [Auteur]
Service de Parasitologie-Mycologie [CHRU LIlle]
Dubuquoy, Laurent [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Soloviev, Dmitry [Auteur]
Cleveland Clinic
Poulain, Daniel [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Sendid, Boualem [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Jawhara, Samir [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Lille Inflammation Research International Center - U 995 [LIRIC]
Charlet, Rogatien [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Guerardel, Yann [Auteur]
Unité de Glycobiologie Structurale et Fonctionnelle UMR 8576 [UGSF]
Choteau, Laura [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Bauters, Anne [Auteur]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Tardivel, Meryem [Auteur]
Université de Lille, Droit et Santé
Francois, Nadine [Auteur]
Service de Parasitologie-Mycologie [CHRU LIlle]
Dubuquoy, Laurent [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Soloviev, Dmitry [Auteur]
Cleveland Clinic
Poulain, Daniel [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Sendid, Boualem [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Jawhara, Samir [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Titre de la revue :
American journal of physiology. Heart and circulatory physiology
Nom court de la revue :
Am. J. Physiol.-Heart Circul. Physiol.
Numéro :
311
Pagination :
H725-H734
Date de publication :
2016-09-01
ISSN :
0363-6135
Mot(s)-clé(s) en anglais :
toll-like receptors
platelets
coagulation
beta-glucans
Candida albicans
aggregation
platelets
coagulation
beta-glucans
Candida albicans
aggregation
Discipline(s) HAL :
Sciences du Vivant [q-bio]
Résumé en anglais : [en]
Platelets are capable of binding, aggregating, and internalizing microorganisms, which enhances the elimination of pathogens from the blood. The yeast Candida albicans is a pathobiont causing life-threatening invasive ...
Lire la suite >Platelets are capable of binding, aggregating, and internalizing microorganisms, which enhances the elimination of pathogens from the blood. The yeast Candida albicans is a pathobiont causing life-threatening invasive infections. Its cell wall contains β-1,3 glucans that are known to trigger a wide range of host cell activities and to circulate during infection. We studied the effect of β-1,3 glucan fractions (BGFs) consisting of diglucosides (Glc2), tetraglucosides (Glc4), and pentaglucosides (Glc5) on human platelets, their mechanisms of action, and their possible impact on host defenses. The effect of BGFs on the coagulation process was determined by measuring thrombin generation. Platelets pretreated with BGFs were analyzed in terms of activation, receptor expression, aggregation, and adhesion to neutrophils and to C. albicans. The results show that BGFs affected the endogenous thrombin potential in a concentration-dependent manner. For platelet activation, BGFs at a low concentration (2 μmol/l) reduced ATP release and prevented the phosphorylation of protein kinase C. BGFs diminished the expression of P-selectin and the activation of αIIbβ3. BGFs decreased platelet aggregation and the interaction between thrombin-stimulated platelets and neutrophils, fibrinogen, and C. albicans. GLc5 decreased ATP release and TGF-β1 production in response to TLR4 upregulation in thrombin-stimulated platelets, but TLR4 blockage abolished the effect of BGFs on platelets. This study provides evidence that fungal pentaglucosides modulate platelet activity mediated via TLR4 stimulation and reduce platelet-neutrophil interaction.Lire moins >
Lire la suite >Platelets are capable of binding, aggregating, and internalizing microorganisms, which enhances the elimination of pathogens from the blood. The yeast Candida albicans is a pathobiont causing life-threatening invasive infections. Its cell wall contains β-1,3 glucans that are known to trigger a wide range of host cell activities and to circulate during infection. We studied the effect of β-1,3 glucan fractions (BGFs) consisting of diglucosides (Glc2), tetraglucosides (Glc4), and pentaglucosides (Glc5) on human platelets, their mechanisms of action, and their possible impact on host defenses. The effect of BGFs on the coagulation process was determined by measuring thrombin generation. Platelets pretreated with BGFs were analyzed in terms of activation, receptor expression, aggregation, and adhesion to neutrophils and to C. albicans. The results show that BGFs affected the endogenous thrombin potential in a concentration-dependent manner. For platelet activation, BGFs at a low concentration (2 μmol/l) reduced ATP release and prevented the phosphorylation of protein kinase C. BGFs diminished the expression of P-selectin and the activation of αIIbβ3. BGFs decreased platelet aggregation and the interaction between thrombin-stimulated platelets and neutrophils, fibrinogen, and C. albicans. GLc5 decreased ATP release and TGF-β1 production in response to TLR4 upregulation in thrombin-stimulated platelets, but TLR4 blockage abolished the effect of BGFs on platelets. This study provides evidence that fungal pentaglucosides modulate platelet activity mediated via TLR4 stimulation and reduce platelet-neutrophil interaction.Lire moins >
Langue :
Anglais
Audience :
Internationale
Vulgarisation :
Non
Établissement(s) :
Inserm
Université de Lille
CHU Lille
CNRS
Université de Lille
CHU Lille
CNRS
Collections :
Équipe(s) de recherche :
Inflammatory digestive disease : pathophysiology and therapeutic targets developement
Fungal associated invasive and inflammatory diseases
Fungal associated invasive and inflammatory diseases
Date de dépôt :
2019-03-01T15:16:18Z
2021-03-25T08:15:25Z
2021-06-08T13:03:36Z
2021-03-25T08:15:25Z
2021-06-08T13:03:36Z