XXXX and pathological damage to the lungs of @entity19 are only partially reversed following smoking cessation on subacute exposure to cigarette smoke.

@entity32 @entity1236 @entity19 @entity641 @entity358 @entity1030
UNASSIGNED: The present study aimed to observe the level of @entity32 and the number of lesions in the airways and parenchyma of @entity19 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 @entity1236 and transforming growth factor (TGF)  -b1 were detected in the airways and @entity358 of C57BL/6  J @entity19 . @entity19 , 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    m 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 @entity1236 and @entity641 increased in the airways following 4  weeks smoke exposure, however, there was no further increase at 8  weeks, and the expression levels of @entity641 in the @entity358 decreased. At 4  weeks post  -smoking cessation, the expression levels of @entity641 in the airways and @entity358 returned to normal; whereas, 1  week after smoking cessation, the expression levels of @entity1236 were higher compared with the normal control group. Subacute exposure to cigarette smoke induced an inflammatory response and regional damage to the @entity358 , 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 @entity1236 remained significantly higher compared with the control @entity19 . These results suggested that regulation of the expression of @entity1236 and @entity641 , particularly in the distribution in the airways and @entity358 , may be a strategy for the early treatment of @entity1030 .
