Immunohistochemical study of tumor necrosis factor-alpha, matrix metalloproteinase-12, and tissue inhibitor of metalloproteinase-2 on alveolar macrophages of BALB/c mice exposed to short-term cigarette smoke.

Alveolar cells were evaluated in BALB/c mice exposed to smoke from 9 cigarettes per day. The mice were sacrificed at 1, 5, and 10 days and examined by lung morphometry and immunohistochemical staining of alveolar macrophages for tumor necrosis factor (TNF)-alpha, matrix metalloproteinase (MMP)-12, and tissue inhibitor of metalloproteinase (TIMP)-2. Cigarette smoke (CS)-exposed mice showed a progressive increase in numbers of alveolar macrophages (AMs) up to 10 days.

Emphysema and metalloelastase expression in mouse lung induced by cigarette smoke.

Cigarette smoke (CS) causes pulmonary emphysema in humans and elastin degradation plays a key role in its pathogenesis. Previous studies on CS-exposed animals have been equivocal and have not clearly demonstrated the progression of the disease. In this study, morphometry was used to assess lung modifications to alveolar septa, airspaces, elastic and collagen fibers, and alveolar macrophages.

Lung morphometry and MMP-12 expression in rats treated with intraperitoneal nicotine.

Nicotine, a toxic tobacco component, plays an important role in the development of cardiovascular and lung diseases in smokers. Our objective was to investigate the effects of the intraperitoneal (i.p.