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(Chest. 2000;117:320S.)
© 2000 American College of Chest Physicians

Apoptosis of Alveolar Macrophages by Cigarette Smoke*

Kazutetsu Aoshiba, MD; Shuju Yasui, MD and Atsushi Nagai, MD, FCCP

* From the First Department of Medicine, Tokyo Women’s Medical University, Tokyo, Japan.

Correspondence to: Atsushi Nagai, MD, FCCP, First Department of Medicine, Tokyo Women’s Medical University, 8–1 Kawada-cho, Shinjuku-ku, Tokyo 162-8666, Japan


   Introduction
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 Introduction
 
Abbreviations: AM = alveolar macrophages; CS = cigarette smoke

Apoptosis is a critical mechanism controlling cellularity in various tissues. It is so far unknown whether apoptosis plays a role in cigarette smoking-related pulmonary diseases. It is, however, reported that inhaled toxic materials such as silica and particle matters induce apoptosis of alveolar macrophages (AMs). This study was aimed to test hypothesis that cigarette smoke (CS) may induce apoptosis of AMs. In lung tissue specimens obtained from current smokers with pulmonary emphysema, approximately 0.3% of the AM population were found to be positive for terminal deoxynucleotidyl transferase-mediated nucleotide nick end-labeling and immunostaining with monoclonal anti-single-stranded DNA (ApoStain; Alexis Corp; San Diego, CA). In in vitro studies, mouse, rat, and human AMs, and human blood monocyte-derived macrophages cultured with aqueous cigarette smoke extracts underwent apoptosis as evidenced by light and electron microscopy, and terminal deoxynucleotidyl transferase-mediated nucleotide nick end-labeling. This apoptosis was associated with increased oxidative stress, Bax protein accumulation, mitochondrial dysfunction, and mitochondrial cytochrome c release, but was independent of p53, Fas, and caspase activation. The cigarette smoke extract-induced apoptosis was inhibited by glutathione, ascorbic acid, and {alpha}-tocopherol, which are antioxidants known to be present in respiratory tract lining fluids. In in vivo studies where rats were exposed to the smoke from 10 cigarettes over 5 h in an exposure chamber, approximately 3% of AMs obtained by BAL showed apoptosis after 24 h. To evaluate the role of lung antioxidants in CS-induced AM apoptosis in vivo, glutathione-depleted rats produced by administration of buthionine sulfoximine were exposed to CS. There was a significant increase in CS-induced AM apoptosis in glutathione-depleted rats compared with control rats. These results may provide information to explain macrophage dysfunction and lung diseases in cigarette smokers.




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