7. Neutrophils and Vascular Inflammation

  1. Gary S. Hoffman MD, MS2,
  2. Cornelia M. Weyand MD, PhD3,
  3. Carol A. Langford MD, MHS2 and
  4. Jörg J. Goronzy MD, PhD3
  1. Matthew David Morgan MB, ChB, PhD and
  2. Caroline O. S. Savage PhD, FRCP, FMedSci

Published Online: 3 MAY 2012

DOI: 10.1002/9781118355244.ch7

Inflammatory Diseases of Blood Vessels, Second Edition

Inflammatory Diseases of Blood Vessels, Second Edition

How to Cite

Morgan, M. D. and Savage, C. O. S. (2012) Neutrophils and Vascular Inflammation, in Inflammatory Diseases of Blood Vessels, Second Edition (eds G. S. Hoffman, C. M. Weyand, C. A. Langford and J. J. Goronzy), Wiley-Blackwell, Oxford, UK. doi: 10.1002/9781118355244.ch7

Editor Information

  1. 2

    Department of Rheumatic and Immunologic Diseases, Center for Vasculitis Care and Research, Cleveland Clinic, Lerner College of Medicine, Cleveland, OH, USA

  2. 3

    Department of Medicine, Stanford University School of Medicine, Stanford, CA, USA

Author Information

  1. Renal Immunobiology, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK

Publication History

  1. Published Online: 3 MAY 2012
  2. Published Print: 8 JUN 2012

ISBN Information

Print ISBN: 9781444338225

Online ISBN: 9781118355244

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Keywords:

  • Neutrophil;
  • vasculitis;
  • atheroma;
  • ANCA;
  • protease;
  • superoxide;
  • inflammation;
  • Wegener's granulomatosis;
  • cytokine

Summary

Neutrophils contribute to the development of vascular inflammation by the generation of reactive oxygen and nitrogen species, release of proteases and cytokines. This leads to the damage and death of endothelial and tissue cells, destruction of extracellular matrix, further recruitment of leukocytes and modification of leukocyte and tissue cell behavior. They have an important role in antineutrophil cytoplasm antibody associated vasculitis and Kawasaki's disease and probably less important roles in other forms of primary vasculitis. They also contribute to the development of plaque instability in atheromatous disease leading to plaque rupture and ischemic events.