Inhibitor activity against elastolytic enzymes in the bronchial area. A contribution to the pathogenesis of chronic airway obstruction

Abstract

In the bronchial mucus of patients with long-term airway obstruction free elastolytic activities are observed. These originate from leucocytes with polymorphous nuclei and may cause the digestion of lung tissue and thus an emphysematous lung metaplasia. It is known that the supersensitivity of bronchial musculature increases due to the influence of proteolytic ferments. For the inhibition of elastolytic enzymes, specific, acid-proof, low-molecular inhibitory substances are available. We were able to measure three of them in bronchial mucus against different substrates; i.e. against substrates for trypsin, pancreas elastase and leucocyte elastase. Our results show that the free inhibitor preparation decreases if free elastolytic activity in bronchial mucus is measured and is no longer available if the concentration decreases. It was also found that the concentration of secretory IGA decreases if the elastolytic activity increases. Thus, it is possible that the secretory IGA molecule is attacked by proteolytic enzymes. It is known that in case of chronic obstructive airway diseases lysozyme is released from leucocytes with polymorphous nuclei; in case of silicosis, from macrophages as well. In this study, the lysozyme concentration served as measurement for cell decomposition. The observation showed that in spite of the same lysozyme levels the elastolytic activity in patients can be very different. It is in strong connection with the available inhibitor capacity. Regarding the clinical evaluation can be concluded that some patients show a lack of secretory inhibitors. On a long-term basis, this lack can lead to the formation of emphysemata.