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A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
Published on: May 6, 2014
Neutrophils in atherosclerosis: from mice to man
Yvonne Döring1, Maik Drechsler1, Oliver Soehnlein1
1From the Institute for Cardiovascular Prevention, Ludwig-Maximilians-University Munich, Munich, Germany (Y.D., M.D., O.S., C.W.); Department of Pathology, Academic Medical Center, Amsterdam University, Amsterdam, The Netherlands (M.D., O.S.); and German Centre for Cardiovascular Research (DZHK), Partner Site Munich Heart Alliance, Munich, Germany (O.S., C.W.).
Abstract:
Infiltration of leukocyte subsets is a driving force of atherosclerotic lesion growth, and during the past decade, neutrophils have received growing attention in chronic inflammatory processes, such as atherosclerosis. Equipped with various ready to be released mediators, evolved to fight invading pathogens, neutrophils may also hold key functions in affecting sterile inflammation, such as in atherosclerosis. Many of their secretion products might instruct or activate other immune cells (particularly monocytes) to, for example, enter atherosclerotic lesions or release proinflammatory mediators. Despite the emerging evidence for the mechanistic contribution of neutrophils to early atherosclerosis in mice, their role in human atherogenesis, atheroprogression, and atherosclerotic plaque destabilization is still poorly understood. This brief review will summarize latest findings on the role of neutrophils in atherosclerosis and will pay special attention to studies describing a translation approach by combining measurements in mouse and human.
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