STIMULATORY EFFECT OF INFLAMMATORY CYTOKINES ON ALPHA(1)-ANTICHYMOTRYPSIN EXPRESSION IN HUMAN LUNG-DERIVED EPITHELIAL-CELLS

Although it is a well known fact that hepatocytes are the primary source of plasma proteinase inhibitors, including alpha(1)-antichymotrypsin, this protein has also been detected in lung epithelial cells, which may suggest its local production, We have demonstrated that lung-derived epithelial cells are capable of synthesizing high levels of alpha(1)-antichymotrypsin. In normal bronchial epithelial cells, as well as in the HTB55 human adenocarcinoma cell line, alpha(1)-antichymotrypsin synthesis was under the control of inflammatory cytokines, of which oncostatin M was the most potent stimulator. This finding is consistent with a role for this inhibitor in protecting the lung epithelium from damage by chymotrypsinlike enzymes released from phagocytes such as neutrophils following pathogen invasion.