TREM-1 inhibition restores impaired autophagy activity and reduces colitis in mice.

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

https://www.ncbi.nlm.nih.gov/pubmed/28961797

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;: