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[Proteases, antiproteases and pulmonary emphysema]
Revue Francaise Des Maladies Respiratoires
|January 1, 1982
Summary
Emphysema is linked to an imbalance between proteases and antiproteases in the lungs. Factors like smoking and infection increase proteases, overwhelming natural inhibitors and damaging lung tissue.
Area of Science:
- Pulmonary Medicine
- Biochemistry
Background:
- Alpha 1 antiprotease deficiency is linked to early-onset emphysema.
- Emphysema can be experimentally induced by elastolytic proteases, suggesting a protease-antiprotease imbalance.
Purpose of the Study:
- Investigate the roles of various proteases (leukocyte, macrophage, microbial) in emphysema development.
- Contrast the inhibitory actions of alpha 1 antiprotease and bronchial inhibitors against these proteases.
- Discuss the influence of irritants on the protease-antiprotease equilibrium in the lungs.
Main Methods:
- Analysis of protease and antiprotease activities in bronchial secretions and bronchoalveolar lavage.
- Review of existing literature on protease roles and inhibitor functions.
Main Results:
- Leukocyte elastase is strongly implicated in emphysema genesis.
- Tobacco smoke, infection, and phagocyte activation promote leukocyte elastase release.
- Protease activity can inactivate alpha 1 antiproteases and bronchial inhibitors, altering the lung's protease-antiprotease balance.
Conclusions:
- Emphysema arises from an imbalance favoring proteases over antiproteases in the pulmonary system.
- Environmental factors significantly disrupt this balance, contributing to emphysema pathogenesis.
- Changes in elastolytic and anti-elastolytic activity in secretions reflect this imbalance.