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

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State: Public
Version: Final published version
Serval ID
serval:BIB_CD66AE8EFD9F
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
TREM-1 links dyslipidemia to inflammation and lipid deposition in atherosclerosis.
Journal
Nature communications
Author(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
Publication state
Published
Issued date
20/10/2016
Peer-reviewed
Oui
Volume
7
Pages
13151
Language
english
Abstract
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
Yes
Create date
01/11/2016 19:28
Last modification date
20/08/2019 15:48
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