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 chymotrypsin-like enzymes released from phagocytes such as neutrophils following pathogen invasion.
Cichy
J
J
Department of Microbiology and Immunology, Jagiellonian University, Kraków, Poland.
Potempa
J
J
Chawla
R K
RK
Travis
J
J
D000230:Adenocarcinoma / Q000473:pathology; D001980:Bronchi / Q000378:metabolism; D016207:Cytokines / Q000494:pharmacology*; D003907:Dexamethasone / Q000494:pharmacology; D004848:Epithelium / Q000201:enzymology; D015870:Gene Expression / Q000187:drug effects; D006801:Humans; D066298:In Vitro Techniques; D007249:Inflammation / Q000503:physiopathology; D008168:Lung / Q000201:enzymology*; D053683:Oncostatin M; D010455:Peptides / Q000494:pharmacology; D012333:RNA, Messenger / Q000235:genetics; D014407:Tumor Cells, Cultured; D000514:alpha 1-Antichymotrypsin / Q000378:metabolism*
D016207:Cytokines; C508351:OSM protein, human; D010455:Peptides; D012333:RNA, Messenger; D000514:alpha 1-Antichymotrypsin; D053683:Oncostatin M; D003907:Dexamethasone