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Chronic obstructive pulmonary disease: molecular and cellularmechanisms

P.J. Barnes, S.D. Shapiro, R.A. Pauwels
European Respiratory Journal 2003 22: 672-688; DOI: 10.1183/09031936.03.00040703
P.J. Barnes
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S.D. Shapiro
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R.A. Pauwels
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Abstract

Chronic obstructive pulmonary disease is a leading cause of death and disability, but has only recently been extensively explored from a cellular and molecular perspective.

There is a chronic inflammation that leads to fixed narrowing of small airways and alveolar wall destruction (emphysema). This is characterised by increased numbers of alveolar macrophages, neutrophils and cytotoxic T‐lymphocytes, and the release of multiple inflammatory mediators (lipids, chemokines, cytokines, growth factors). A high level of oxidative stress may amplify this inflammation. There is also increased elastolysis and evidence for involvement of several elastolytic enzymes, including serine proteases, cathepsins and matrix metalloproteinases.

The inflammation and proteolysis in chronic obstructive pulmonary disease is an amplification of the normal inflammatory response to cigarette smoke. This inflammation, in marked contrast to asthma, appears to be resistant to corticosteroids, prompting a search for novel anti-inflammatory therapies that may prevent the relentless progression of the disease.

  • chemokine
  • cytokine
  • emphysema
  • macrophage
  • oxidative stress
  • protease

The meeting “COPD: the important questions” held in Malta in November 2002 was sponsored by AstraZeneca.

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Chronic obstructive pulmonary disease: molecular and cellularmechanisms
P.J. Barnes, S.D. Shapiro, R.A. Pauwels
European Respiratory Journal Oct 2003, 22 (4) 672-688; DOI: 10.1183/09031936.03.00040703

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Chronic obstructive pulmonary disease: molecular and cellularmechanisms
P.J. Barnes, S.D. Shapiro, R.A. Pauwels
European Respiratory Journal Oct 2003, 22 (4) 672-688; DOI: 10.1183/09031936.03.00040703
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    • Abstract
    • Differences from asthma
    • What are the predominant mechanisms of airflow limitation?
    • What are the key inflammatory cells?
    • What is the role of oxidative stress?
    • Which proteases are important?
    • What are the amplifying mechanisms?
    • Why is there a poor response to corticosteroids?
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More in this TOC Section

  • Core Outcome Measures sets for paediatric and adult Severe Asthma
  • Identifying outcome measures for severe asthma
  • Cystic fibrosis transmembrane conductance regulator in COPD
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