TREM-1 inhibition restores impaired autophagy activity and reduces colitis in mice.
Fiche publication
Date publication
septembre 2017
Journal
Journal of Crohn's & colitis
Auteurs
Membres identifiés du Cancéropôle Est :
Pr GUEANT Jean-Louis, Pr JOUZEAU Jean-Yves, Pr MULLER Sylviane
Tous les auteurs :
Kökten T, Gibot S, Lepage P, D'Alessio S, Hablot J, Ndiaye NC, Busby-Venner H, Monot C, Garnier B, Moulin D, Jouzeau JY, Hansmannel F, Danese S, Guéant JL, Muller S, Peyrin-Biroulet L
Lien Pubmed
Résumé
Triggering receptor expressed on myeloid cells-1 [TREM-1] is known to amplify inflammation in several diseases. Autophagy and endoplasmic reticulum [ER] stress, which activates the unfolded protein response [UPR] are closely linked and defects in these pathways contribute to the pathogenesis of inflammatory bowel disease [IBD]. Both autophagy and UPR are deeply involved in host-microbiota interactions for the clearance of intracellular pathogens thus contributing to dysbiosis. We investigated whether inhibition of TREM-1 would prevent aberrant inflammation by modulating autophagy, ER stress and preventing dysbiosis.
Mots clés
Animal models of IBD, LR12 peptide, TREM-1, autophagy, dysbiosis, endoplasmic reticulum stress, endoscopy, inflammation, inflammatory bowel disease, innovative therapy, peptide-based therapy
Référence
J Crohns Colitis. 2017 Sep;: