Inflammation and pathological damage to the lungs of mice are only partially reversed following smoking cessation on subacute exposure to cigarette smoke

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.