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

Daniel Zysset, Benjamin Weber, Silvia Rihs, Jennifer Brasseit, Stefan Freigang, Carsten Riether, Yara Banz, Adelheid Cerwenka, Cedric Simillion, Pedro Marques-Vidal, Adrian F. Ochsenbein, Leslie Saurer () and Christoph Mueller ()
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Daniel Zysset: Institute of Pathology, University of Bern
Benjamin Weber: Institute of Pathology, University of Bern
Silvia Rihs: Institute of Pathology, University of Bern
Jennifer Brasseit: Institute of Pathology, University of Bern
Stefan Freigang: Institute of Pathology, University of Bern
Carsten Riether: Tumor Immunology, University of Bern
Yara Banz: Institute of Pathology, University of Bern
Adelheid Cerwenka: Innate Immunity Group, German Cancer Research Center
Cedric Simillion: Tumor Immunology, University of Bern
Pedro Marques-Vidal: Internal Medicine, Lausanne University Hospital
Adrian F. Ochsenbein: Tumor Immunology, University of Bern
Leslie Saurer: Institute of Pathology, University of Bern
Christoph Mueller: Institute of Pathology, University of Bern

Nature Communications, 2016, vol. 7, issue 1, 1-16

Abstract: 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.

Date: 2016
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DOI: 10.1038/ncomms13151

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