title: Lack of neutrophil-derived CRAMP reduces atherosclerosis in mice.
abstract: BACKGROUND
  Neutrophils have been reported to contribute to early atherosclerotic lesion formation. Mechanisms of neutrophil-driven atherosclerosis remain unclear so far.
  
  
  OBJECTIVE
  Investigation of the role of the neutrophil granule protein cathelicidin (CRAMP in mouse, LL37 in human) in atherosclerosis.
  
  
  RESULTS
  Compared to Apoe(-/-) mice, Cramp(-/-) Apoe(-/-) mice exhibit reduced lesion sizes with lower macrophage numbers. In atherosclerotic aortas, we could detect CRAMP specifically in neutrophils, but not in monocytes or macrophages. By use of intravital microscopy, CRAMP was found to be deposited by activated neutrophils on inflamed endothelium of large arteries. In this location cathelicidins promote adhesion of classical monocytes and neutrophils, but not nonclassical monocytes in a formyl-peptide receptor-dependent manner.
  
  
  CONCLUSIONS
  Cathelicidins promote atherosclerosis by enhancement of the recruitment of inflammatory monocytes.
authors.affiliation: Institute for Cardiovascular Prevention, Ludwig-Maximilians University München, Munich, Germany.
authors.forename: Yvonne
authors.initials: Y
authors.lastname: Döring
authors.forename: Maik
authors.initials: M
authors.lastname: Drechsler
authors.forename: Sarawuth
authors.initials: S
authors.lastname: Wantha
authors.forename: Klaus
authors.initials: K
authors.lastname: Kemmerich
authors.forename: Dirk
authors.initials: D
authors.lastname: Lievens
authors.forename: Santosh
authors.initials: S
authors.lastname: Vijayan
authors.forename: Richard L
authors.initials: RL
authors.lastname: Gallo
authors.forename: Christian
authors.initials: C
authors.lastname: Weber
authors.forename: Oliver
authors.initials: O
authors.lastname: Soehnlein
mesh_terms: D000818:Animals; D023181:Antimicrobial Cationic Peptides; D001011:Aorta / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D001018:Aortic Diseases / Q000235:genetics / Q000276:immunology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D001057:Apolipoproteins E / Q000172:deficiency / Q000235:genetics; D050197:Atherosclerosis / Q000235:genetics / Q000276:immunology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D054804:Cathelicidins / Q000172:deficiency* / Q000235:genetics; D002448:Cell Adhesion; D002478:Cells, Cultured; D002634:Chemotaxis, Leukocyte; D018920:Coculture Techniques; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000276:immunology / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000235:genetics / Q000276:immunology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008856:Microscopy, Fluorescence; D009000:Monocytes / Q000276:immunology / Q000378:metabolism; D009504:Neutrophils / Q000276:immunology / Q000378:metabolism*; D013997:Time Factors
chemical_list: D023181:Antimicrobial Cationic Peptides; D001057:Apolipoproteins E; D054804:Cathelicidins