• Y Nakamura, D J Romberger, L Tate, R F Ertl, M Kawamoto, Y Adachi, T Mio, J H Sisson, J R Spurzem, and S I Rennard.
• University of Nebraska Medical Center, Omaha 68198-5300, USA.
• Am. J. Respir. Crit. Care Med. 1995 May 1; 151 (5): 149715031497-503.

AbstractCigarette smoking is the most clearly recognized cause of pulmonary emphysema. Since loss of lung tissue, which characterizes emphysema, represents a balance between injury and repair, we hypothesized that cigarette smoke might contribute to the development of emphysema by inhibiting fibroblast proliferation and migration. To evaluate this, we examined the effect of cigarette smoke extract (CSE) on the proliferation and migration of human lung fibroblasts in vitro. CSE inhibited fibroblast proliferation and migration at noncytotoxic concentrations. When CSE was treated to remove volatile components, it showed less inhibitory activity on fibroblast proliferation. Therefore, we also examined acrolein and acetaldehyde, which are volatile components of cigarette smoke, Micromolar concentrations of acrolein and millimolar concentrations of acetaldehyde induced significant inhibition of fibroblast proliferation. In contrast, removal of volatile components did not eliminate the inhibitory activity of CSE for fibroblast migration, although acetaldehyde and acrolein alone were also capable of inhibiting chemotaxis. Cigarette smoke-induced inhibition of fibroblast proliferation and migration may impair lung repair following lung injury, and may thus contribute to the development of pulmonary emphysema.

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