[Proteases, antiproteases and pulmonary emphysema].

A deficiency of alpha 1 antiproteases is associated with severe and early emphysema. This emphysema can be experimentally produced in animals by endotracheal instillation of elastolytic proteases. Thus it would seem that emphysema is linked to an imbalance between proteases and antiproteases at the pulmonary level. This work studies the proteases, whose role in the genesis of emphysema is highly probable in view of the data in the literature (leukocyte elastase), disputed (macrophage elastase) or transitory (microbial elastases). We contrast the main agents capable of inhibiting these proteases (alpha 1 antiprotease and bronchial inhibitors) or of changing their activity (alpha 2 macroglobulins). The relative importance of these antiproteases is discussed in the light of studies made on bronchial secretions and bronchoalveolar lavage. These irritants may influence the protease - antiprotease equilibrium and favour the development of emphysema by increasing the proteases or decreasing the antiproteases. It appears that tobacco, as well as infection and anything which sets in motion the pulmonary phagocytes favour the liberation of leucocyte elastase. These attacks inactive the alpha 1 antiproteases in addition to the bronchial inhibitor. They may be recognized by a change in elastolytic and anti-elastolytic activity observed in bronchial secretions and in bronchoalveolar lavage (which is more disputed in the latter).