Damaging role of neutrophil elastase in the elastic fiber and basement membrane in human emphysematous lung.

The immunolocalization of human neutrophil elastase (HNE) in the alveolar interstitium of 6 patients with emphysema was investigated by immunochemical electron microscopy. The results showed that HNE is localized in the azurophil granules of neutrophils, and extracellularly on the elastic fibers of alveolar interstitium and basement membranes of epithelium and endothelium. The damage of elastic fibers and basement membranes could be observed. The HNE level of the alveolar interstitium was obviously elevated and closely related to the severity of emphysematous lesions as shown by measuring the mean linear intercept (MLI) in 4 emphysematous lungs with chronic bronchitis (r = 0.84). This suggests that HNE might play an important role in the pathogenesis of emphysema. Although enlarged airspace and increased MLI data were observed in 2 patients, one with asthma and the other, an elderly patient, without lung diseases, the HNE level of alveolar interstitium is much less than that of the other 4 chronic obstructive pulmonary disease patients. This implies that the mechanism of the the airspace enlargement occurring in the 2 patients may be different from that of others. These findings support the hypothesis of elastase-antielastase imbalance on the pathogenesis of pulmonary emphysema.

Damaging role of neutrophil elastase in the elastic fiber and basement membrane in human emphysematous lung

The immunolocalization of human neutrophil elastase (HNE) in the alveolar interstitium of 6 patients with emphysema was investigated by immunochemical electron microscopy. The results showed that HNE is localized in the azurophil granules of neutrophils, and extracellularly on the elastic fibers of alveolar interstitium and basement membranes of epithelium and endothelium. The damage of elastic fibers and basement membranes could be observed. The HNE level of the alveolar interstitium was obviously elevated and closely related to the severity of emphysematous lesions as shown by measuring the mean linear intercept (MLI) in 4 emphysematous lungs with chronic bronchitis (r = 0.84). This suggests that HNE might play an important role in the pathogenesis of emphysema. Although enlarged airspace and increased MLI data were observed in 2 patients, one with asthma and the other, an elderly patient, without lung diseases, the HNE level of alveolar interstitium is much less than that of the other 4 chronic obstructive pulmonary disease patients. This implies that the mechanism of the the airspace enlargement occurring in the 2 patients may be different from that of others. These findings support the hypothesis of elastase-antielastase imbalance on the pathogenesis of pulmonary emphysema.