Comparison of alveolar macrophage and blood monocyte oxidative burst response in pulmonary sarcoidosis.

The alveolitis of sarcoidosis is dominated by lymphocytes and mononuclear phagocytes and chronic macrophage activation may play a role in the pulmonary interstitial fibrosis of sarcoidosis. We measured superoxide anion release of alveolar macrophages from sarcoidosis patients after in vitro stimulation, as toxic oxygen radicals have been proposed as mediators of chronic tissue damage. In untreated patients alveolar macrophage activity was normal, but significantly lower than in blood monocytes. However, a negative correlation between lymphocytosis in bronchoalveolar lavage fluid and macrophage oxidative metabolism was observed, showing that only patients with high intensity alveolitis have a decreased oxidative burst response after in vitro stimulation. This may reflect in vivo activation of the cells with subsequent reduced ability to respond after additional stimulation in vitro. Patients with radiological stage I had lower alveolar macrophage response than patients in stage II or III. There was no correlation with SACE levels, lung function tests or smoking habits. Nine patients were reinvestigated after treatment with prednisolone. Although the lymphocytosis of lavage fluid was only insignificantly changed, all but one patient showed improved macrophage release of superoxide anion. Blood monocyte oxidative burst response was normal in all patients before and after treatment. In conclusion, only mononuclear phagocytes of the target organ (lung) showed an altered function and the most pronounced decrease was observed in sarcoid patients with active alveolitis. Chronic low grade toxic oxygen radical release of alveolar macrophages may be involved in the pathology of pulmonary sarcoidosis.