Chest
Macrophages and the Pathogenesis of COPD
Section snippets
Macrophages and COPD
Whatever the situation, macrophages are elevated in the lungs of smokers and those patients with COPD, where they accumulate in the alveoli, bronchioli, and small airways. Furthermore, there is a positive association between macrophage numbers in the alveolar walls and the presence of mild-to-moderate emphysema as well as the degree of small airways disease in patients with COPD.1,2 The slow progression and chronicity of COPD parallels the chronic increase of macrophages that is seen at sites
Macrophages and Neutrophils in the Pathogenesis of COPD
Historically, the neutrophil and neutrophil proteinases have been thought to play a major role in the development of emphysema, based on the relationship between α1-antitrypsin deficiency and the predisposition of those affected to develop the disease.3 α1-Antitrypsin (ie, α1-proteinase inhibitor) inhibits neutrophil serine proteinases, especially elastase, and, in turn, neutrophil-derived serine proteinases cleave elastin, the disruption of which may be a significant feature of emphysema.
Proteinases in COPD
If the proteinase hypothesis for the development of emphysema is true, one might hypothesize that the macrophage is responsible.3,7 For > 20 years, studies have demonstrated the release of metalloproteinase activity by macrophages, although the lack of adequate technology long delayed a full understanding of the exact nature of this activity and its contribution to disease processes. More recently, however, a class of proteinases, the MMPs, has been described that accounts for some of the
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