The role of elastases in the development of emphysema

Abstract

Enzymes which degrade elastin can disorganize the network of elastic fibers in the lungs of experimental animals and produce emphysema. Two sources of endogenous elastases in the lung are neutrophils and alveolar macrophages. The neutrophil elastase is an intracellular, granule-associated enzyme which is inhibited by α₁-antitrypsin and has the capacity to produce emphysema in experimental animals. The recently identified macrophage elastase appears to be a secretory enzyme, not associated with granules and less effectively inhibited by α₁-antitrypsin. The demonstration that macrophages from cigarette smokers release elastase in culture, and that cigarette smoke interferes with the action of inhibitors of elastase, suggests that elastases may be involved in the pathogenesis of emphysema in man. Further research is needed to establish whether degradation of elastin occurs in humans developing emphysema.