REGULATION OF ALPHA(1)-ANTICHYMOTRYPSIN SYNTHESIS IN CELLS OF EPITHELIAL ORIGIN

Oncostatin M, interleukin-1 and the glucocorticoid analog, dexamethasone, have been identified as potent stimulators of alpha(1)-antichymotrypsin production in various cells of epithelial origin, Although being able to act individually, these factors exerted a dramatic increase in alpha(1)-antichymotrypsin synthesis when administrated in combination. Their stimulatory effect was independent of the levels of constitutive synthesis of this inhibitor, which was already high in lung- and breast- and low in skin-derived epithelial cells. Since alpha(1)-antichymotrypsin controls chymotrypsin-like proteinases which are released during inflammation, these data support the concept that local synthesis of this inhibitor may be important in reducing tissue damage associated with this process.