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Neutrophils are implicated in the pathogenesis of atherosclerosis but are seldom detected in atherosclerotic plaques. We investigated whether neutrophil-derived microvesicles may influence arterial pathophysiology. Here we report that levels of circulating neutrophil microvesicles are enhanced by exposure to a high fat diet, a known risk factor for atherosclerosis. Neutrophil microvesicles accumulate at disease-prone regions of arteries exposed to disturbed flow patterns, and promote vascular inflammation and atherosclerosis in a murine model. Using cultured endothelial cells exposed to disturbed flow, we demonstrate that neutrophil microvesicles promote inflammatory gene expression by delivering  miR-155,  enhancing NF-κB activation. Similarly, neutrophil microvesicles increase  miR-155  and enhance NF-κB at disease-prone sites of disturbed flow in vivo. Enhancement of atherosclerotic plaque formation and increase in macrophage content by neutrophil microvesicles is dependent on  miR-155 . We conclude that neutrophils contribute to vascular inflammation and atherogenesis through delivery of microvesicles carrying  miR-155  to disease-prone regions.

Neutrophil microvesicles drive atherosclerosis by delivering miR-155 to atheroprone endothelium