Implication of Toll/IL-1 receptor domain containing adapters in -induced inflammation.
Fiche publication
Date publication
mai 2021
Journal
Innate immunity
Auteurs
Membres identifiés du Cancéropôle Est :
Dr BENKIRANE-JESSEL Nadia
Tous les auteurs :
Bugueno IM, Benkirane-Jessel N, Huck O
Lien Pubmed
Résumé
Periodontitis is induced by periodontal dysbiosis characterized by the predominance of anaerobic species. TLRs constitute the classical pathway for cell activation by infection. Interestingly, the Toll/IL-1 receptor homology domain adapters initiate signaling events, leading to the activation of the expression of the genes involved in the host immune response. The aim of this study was to evaluate the effects of on the expression and protein-protein interactions among five TIR adapters (MAL, MyD88, TRIF, TRAM and SARM) in gingival epithelial cells and endothelial cells. It was observed that is able to modulate the signaling cascades activated through its recognition by TLR4/2 in gingival epithelial cells and endothelial cells. Indeed, MAL-MyD88 protein-protein interactions associated with TLR4 was the main pathway activated by infection. When transient siRNA inhibition was performed, cell viability, inflammation, and cell death induced by infection decreased and such deleterious effects were almost absent when MAL or TRAM were targeted. This study emphasizes the role of such TIR adapter proteins in elicited inflammation and the precise evaluation of TIR adapter protein interactions may pave the way for future therapeutics in both periodontitis and systemic disease with a involvement, such as atherothrombosis.
Mots clés
Periodontitis, TIR, atherosclerosis, dysbiosis, infection, inflammation
Référence
Innate Immun. 2021 May 21;:17534259211013087