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Abstract

See related article, pages 209–217 The importance of inflammation in the initiation and development of atherosclerosis has been extensively studied over the last decades.1,2 In particular, much effort has been devoted to elucidating the role of chemokines and their receptors, which play a central part in the atherogenic immune response. Indeed, interfering with the chemokine–chemokine receptor system emerged as both an exciting tool to dissect the complex inflammatory response and a promising therapeutic target.3 Although participation of other inflammatory cells such as macrophages and T cells is well documented, less attention has been paid to the involvement of neutrophils. Neutrophil infiltrates are seldom observed within human atherosclerotic plaques in comparison with other inflammatory cells. However, neutrophils have been detected at the sites of plaque erosion or rupture on atherectomy specimens from the patients with unstable angina and on autopsy samples from the patients with acute myocardial infarction.4 Moreover, the increase in proinflammatory molecules occurring with coronary artery diseases correlates with the peripheral neutrophil count,5 which, hence, may be useful as a predictor of complex coronary stenosis or myocardial infarction. A histological analysis of human carotid endarterectomy specimens suggested that intraplaque hemorrhage could convey neutrophils into the atherosclerotic lesion, spreading into the necrotic core, thus participating in its protease enrichment.6 Although these clinical studies have suggested the potential contribution of neutrophils to plaque progression and vulnerability, few animal studies have been performed to determine the role of neutrophils in the pathogenesis of atherosclerosis. The molecular mechanism by which neutrophils accumulate at the advanced plaques remains largely unknown. In the current issue of Circulation Research , Zernecke …