Cigarette smoking increases the numbers and oxidative metabolism of alveolar macrophages. Increased production of Superoxide (O2-) and H2O2 by alveolar macrophages may contribute to the pathogenesis of cigarette-induced lung diseases. The cytotoxlcity mediated by alveolar macrophages from smokers (n = 11) and nonsmokers (n = 13) was compared in an in vitro assay in which the target cells were chromium 51-labeled lung expiants. The spontaneous cellular cytotoxiclty mediated by smoker macrophages was significantly greater than that of nonsmoker macrophages (cytotoxic index 20.3% ± 1.9% compared with 5.5% ± 0.9%, P < 0.001). Phorbol myristate acetate significantly increased the cytotoxic index of nonsmoker macrophages but did not cause further increases in smoker macrophage killing. The antioxidants Superoxide dismutase and catalase produced partial inhibition of smoker macrophage cytotoxicity, suggesting that target cell killing was mediated in part by oxidant mechanisms. Supplementation of smokers' diets with high-dose oral vitamin E failed to decrease smoker alveolar macrophage cytotoxicity. These findings demonstrate that smoker alveolar macrophages possess enhanced cytotoxic potential for normal lung parenchymal cells.
|Original language||English (US)|
|Number of pages||6|
|Journal||Journal of Laboratory and Clinical Medicine|
|State||Published - Jan 1 1988|
ASJC Scopus subject areas
- Pathology and Forensic Medicine