Yonago Acta medica 1997;40:43–52
Cadmium Induces Interleukin-8 in Alveolar Epithelial Type II Cells (A549)
Katsuhiko Fukuda, Yutaka Hitsuda and Tadashi Igishi
Third Department of Internal Medicine, Faculty of Medicine, Tottori University, Yonago 683, Japan
Cadmium (Cd) is a contaminant in cigarette smoke and may play an important role in
the pathogenesis of smoking-related emphysema. It is reported that repeated Cd
exposure causes emphysema after neutrophil infiltration in
the rat lung. Interleukin-8 (IL-8) is a major neutrophil chemotactic factor commonly involved in a variety of
pulmonary disorders including emphysema. The aim of this study is to elucidate the
effect of Cd on IL-8 production of alveolar epithelial type II cells, using the A549 cell
line. We used 1 to 100 µM of cadmium chloride
(CdCl2) to stimulate the cells for a 48 h period. IL-8 production (2957 ± 137 pg/mL) without any cytotoxic effect was observed
in the cell supernatants after 24 h exposure to 50 µM
CdCl2. The Cd-removed supernatant caused neutrophil chemotaxis and was inhibited by the anti-IL-8 antibody.
Cd-induced IL-8 was inhibited by EDTA, and the inhibition was blocked by copper (II)
chloride. The addition of anti-interleukin-1β or tumor necrosis
factor-α antibodies did not diminish IL-8 release induced by Cd. These results suggest that Cd increases the
production of IL-8 without any cytotoxic effect in alveolar epithelial cells, which may
be an important factor in the developmental process of cigarette smoking-related
emphysema.
key words: A549; alveolar epithelial type II cell; cadmium chloride; emphysema; interleukin-8
