title: Neutrophils in atherosclerosis: from mice to man.
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.
authors.affiliation: From 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.).
authors.forename: Yvonne
authors.initials: Y
authors.lastname: Döring
authors.affiliation: From 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.).
authors.forename: Maik
authors.initials: M
authors.lastname: Drechsler
authors.affiliation: From 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.).
authors.forename: Oliver
authors.initials: O
authors.lastname: Soehnlein
authors.affiliation: From 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.). chweber@med.lmu.de.
authors.forename: Christian
authors.initials: C
authors.lastname: Weber
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D004195:Disease Models, Animal; D006801:Humans; D007249:Inflammation / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D018836:Inflammation Mediators / Q000378:metabolism; D051379:Mice; D009504:Neutrophils / Q000276:immunology* / Q000378:metabolism; D010641:Phenotype; D015398:Signal Transduction; D057170:Translational Research, Biomedical
chemical_list: D018836:Inflammation Mediators
keywords: atherosclerosis; inflammation; leukocyte