抄録
The superoxide anion (O-2) release from circulating neutrophils (c-PMN) in interstitial lung diseases, idiopathic interstitial pneumonitis (IIP), sarcoidosis (SA) and rheumatic pneumonitis (RA) was studied. At the same time, we demonstrated that the mechanism of acceleration of phorbol myristate acetate (PMA) -induced O-2 release in c-PMN by using animal model of bleomycin (BLM) -induced lung injury and pulmonary fibrosis. (1) Spontaneous O-2 release was not differ from healthy volunteer group and TIP, RA, SA groups. (2) Time course of PMA-induced O-2 release from c-PMN in TIP was increased significantly compared with that of healthy volunteer, RA and SA groups. (3) f-MLP-induced O-2 release of c-PMN in TIP group was lower than that of healthy volunteer group. (4) On the stage of acute inflammation induced by intratracheal injection of BLM to guinea pigs, f-MLP and alpha-TNF-induced O-2 release from c-PMN in BLM group were increased significantly, but not in spontaneous and PMA stimulation. (5) On the progress stage of BLM-induced fibrosis, various stimulants-induced and spontaneous O-2 release were not differ from saline injected group and BLM group.
These results suggested that c-PMN in IIP patients may affect in pathogenesis of interstitial pulmonary fibrosis which was under the stable stage. And this accelerated PMA-dependent O-2 release could be induced by the change of intracellular signal pathways which transmitted from protein kinase C stimulation to NADPH oxidase activation.
