Alpha-1 antichymotrypsin is increased in human alveolar macrophages by phorbol myristate acetate or lipopolysaccharide and released from these activated macrophages by glucocorticoid.

Alveolar macrophages were obtained from 23 patients and the effects of phorbol myristate acetate (PMA), lipopolysaccharide (LPS), and dexamethasone (DEX) on the proportion of cells with intracellular alpha-1 antichymotrypsin (ACT), and concentrations of ACT in the culture medium were studied in vitro. The alveolar macrophages were obtained by bronchoalveolar lavage at autopsy or from resected lungs at operation and were cultured in suspension for 3 days in medium containing PMA, LPS, DEX, PMA+DEX, or LPS+DEX. Both PMA and LPS significantly increased the percentage of macrophages with intracellular ACT. Dexamethasone did not increase the number of ACT-positive cells and significantly suppressed the increase induced by PMA or LPS, releasing ACT into the culture medium. The release of ACT from macrophages may contribute to the anti-inflammatory effects of corticoids.