TREM-1 links dyslipidemia to inflammation and lipid deposition in atherosclerosis.

Détails

Ressource 1Télécharger: ncomms13151.pdf (1979.15 [Ko])
Etat: Public
Version: Final published version
ID Serval
serval:BIB_CD66AE8EFD9F
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
TREM-1 links dyslipidemia to inflammation and lipid deposition in atherosclerosis.
Périodique
Nature communications
Auteur(s)
Zysset D., Weber B., Rihs S., Brasseit J., Freigang S., Riether C., Banz Y., Cerwenka A., Simillion C., Marques-Vidal P., Ochsenbein A.F., Saurer L., Mueller C.
ISSN
2041-1723 (Electronic)
ISSN-L
2041-1723
Statut éditorial
Publié
Date de publication
20/10/2016
Peer-reviewed
Oui
Volume
7
Pages
13151
Langue
anglais
Résumé
Triggering receptor expressed on myeloid cells-1 (TREM-1) is a potent amplifier of pro-inflammatory innate immune responses, but its significance in non-infectious diseases remains unclear. Here, we demonstrate that TREM-1 promotes cardiovascular disease by exacerbating atherosclerosis. TREM-1 is expressed in advanced human atheromas and is highly upregulated under dyslipidemic conditions on circulating and on lesion-infiltrating myeloid cells in the Apoe(-/-) mouse model. TREM-1 strongly contributes to high-fat, high-cholesterol diet (HFCD)-induced monocytosis and synergizes with HFCD serum-derived factors to promote pro-inflammatory cytokine responses and foam cell formation of human monocyte/macrophages. Trem1(-/-)Apoe(-/-) mice exhibit substantially attenuated diet-induced atherogenesis. In particular, our results identify skewed monocyte differentiation and enhanced lipid accumulation as novel mechanisms through which TREM-1 can promote atherosclerosis. Collectively, our findings illustrate that dyslipidemia induces TREM-1 surface expression on myeloid cells and subsequently synergizes with TREM-1 to enhance monopoiesis, pro-atherogenic cytokine production and foam cell formation.

Pubmed
Open Access
Oui
Création de la notice
01/11/2016 20:28
Dernière modification de la notice
20/08/2019 16:48
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