Bacterial flagellin triggers cardiac innate immune responses and acute contractile dysfunction.

Détails

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Etat: Public
Version: de l'auteur
ID Serval
serval:BIB_24C847D7ADAF
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Bacterial flagellin triggers cardiac innate immune responses and acute contractile dysfunction.
Périodique
Plos One
Auteur(s)
Rolli J., Rosenblatt-Velin N., Li J., Loukili N., Levrand S., Pacher P., Waeber B., Feihl F., Ruchat P., Liaudet L.
ISSN
1932-6203[electronic], 1932-6203[linking]
Statut éditorial
Publié
Date de publication
2010
Volume
5
Numéro
9
Pages
e12687
Langue
anglais
Résumé
BACKGROUND: Myocardial contractile failure in septic shock may develop following direct interactions, within the heart itself, between molecular motifs released by pathogens and their specific receptors, notably those belonging to the toll-like receptor (TLR) family. Here, we determined the ability of bacterial flagellin, the ligand of mammalian TLR5, to trigger myocardial inflammation and contractile dysfunction.
METHODOLOGY/PRINCIPAL FINDINGS: TLR5 expression was determined in H9c2 cardiac myoblasts, in primary rat cardiomyocytes, and in whole heart extracts from rodents and humans. The ability of flagellin to activate pro-inflammatory signaling pathways (NF-kappaB and MAP kinases) and the expression of inflammatory cytokines was investigated in H9c2 cells, and, in part, in primary cardiomyocytes, as well as in the mouse myocardium in vivo. The influence of flagellin on left ventricular function was evaluated in mice by a conductance pressure-volume catheter. Cardiomyocytes and intact myocardium disclosed significant TLR5 expression. In vitro, flagellin activated NF-kappaB, MAP kinases, and the transcription of inflammatory genes. In vivo, flagellin induced cardiac activation of NF-kappaB, expression of inflammatory cytokines (TNF alpha, IL-1 beta, IL-6, MIP-2 and MCP-1), and provoked a state of reversible myocardial dysfunction, characterized by cardiac dilation, reduced ejection fraction, and decreased end-systolic elastance.
CONCLUSION/SIGNIFICANCE: These results are the first to indicate that flagellin has the ability to trigger cardiac innate immune responses and to acutely depress myocardial contractility.
Mots-clé
toll-like receptor-5, myocardial inflammation, signaling pathway, septic shock, cutting edge, sepsis, peroxynitrite, expression, heart, lipopolysaccharide
Pubmed
Web of science
Open Access
Oui
Création de la notice
07/10/2010 13:18
Dernière modification de la notice
20/08/2019 14:03
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