Release of superoxide anion by alveolar macrophages in pulmonary sarcoidosis.

Biological mechanisms involving nonprotease factors mediate the alterations of the alveolar structures which lead to the interstitial fibrosis of pulmonary sarcoidosis. Thus, we have investigated the production of oxidant species by BAL cells from 50 sarcoidosis patients and 18 healthy controls using a lucigenin-dependent CL method. Spontaneous and PMA-induced CL's were significantly higher in untreated patients and treated patients than in spontaneously cured patients or healthy controls (p less than .05). SOD inhibits 60 to 75% of spontaneous CL and 91 to 93% of PMA-induced CL. There was no apparent correlation between the CL of AM's and the radiological types, SACE levels, and gallium scans. In marked contrast, CL was significantly higher in patients with increased alveolar lymphocytosis (greater than or equal to 18%) than in patients with normal BAL. Since there were neither neutrophils nor eosinophils in BAL and since lymphocytes do not produce lucigenin-dependent CL, we believe that CL is produced by AM's. CL inhibition by SOD suggests that superoxide anion is involved in the production of CL. The release of both superoxide anion and related radicals may be of importance in the pathogenesis of pulmonary sarcoidosis.