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

Type of publication Peer-reviewed
Publikationsform Original article (peer-reviewed)
Author Zysset Daniel, Weber Benjamin, Rihs Silvia, Brasseit Jennifer, Freigang Stefan, Riether Carsten, Banz Yara, Cerwenka Adelheid, Simillion Cedric, Marques-Vidal Pedro, Ochsenbein Adrian F, Saurer Leslie, Mueller Christoph,
Project Molecular mechanisms of lipid-induced vascular inflammation in atherosclerosis
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Original article (peer-reviewed)

Journal Nature Communications
Volume (Issue) 7
Page(s) 13151
Title of proceedings Nature Communications
DOI 10.1038/ncomms13151

Open Access

Type of Open Access Website


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.