The present study aimed to observe the level of
inflammation and the number of lesions in the airways and parenchyma of mouse lungs subsequent to smoking cessation following 4 weeks exposure to cigarette
smoke. Enlargement of the regional airspaces, deposition of peribronchial
collagen fibers and macrophage infiltration were assessed. In addition, the expression levels of
matrix metalloproteinase (
MMP)‑12 and
transforming growth factor (TGF)‑β1 were detected in the airways and lung parenchyma of C57BL/6 J mice. Mice, which were exposed to filtered air for 4 weeks or cigarette
smoke for 8 weeks were used as control groups. A 4 week duration of
smoke exposure induced the expansion of alveolar spaces ~100 µm from the terminal bronchioles, but without increased deposition of
collagen around the small airways, which was not reversed following smoking cessation. Pulmonary infiltration of macrophages and the
protein expression levels of MMP‑12 and TGF‑β1 increased in the airways following 4 weeks
smoke exposure, however, there was no further increase at 8 weeks, and the expression levels of TGF‑β1 in the lung parenchyma decreased. At 4 weeks post‑smoking cessation, the expression levels of TGF‑β1 in the airways and lung parenchyma returned to normal; whereas, 1 week after smoking cessation, the expression levels of MMP‑12 were higher compared with the normal control group. Subacute exposure to cigarette
smoke induced an inflammatory response and regional damage to the lung parenchyma, prior to deposition of
collagen around the airways. Following smoking cessation, the pulmonary inflammatory reaction was partially reversed, however, macrophage infiltration and the expression levels of MMP‑12 remained significantly higher compared with the control mice. These results suggested that regulation of the expression of MMP‑12 and TGF‑β1, particularly in the distribution in the airways and lung parenchyma, may be a strategy for the early treatment of
chronic obstructive pulmonary disease.