Abstract
Destruction of components of the extracellular matrix of the lung by neutrophil elastase is believed to be a critical event in the development of obstructive lung disease. The local synthesis of alpha1-proteinase inhibitor, the controlling inhibitor of this enzyme, may provide a partial mechanism for neutrophil elastase regulation, especially during inflammation, when proteolytic enzymes are released from phagocytes. In this study, we show that lung-derived epithelial cells not only have the capacity to synthesize functional alpha1-PI but also to increase the rate of its production when stimulated by specific inflammatory mediators, including oncostatin M, interleukin-1, and the glucocorticoid analogue, dexamethasone.
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