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IMMUNOHISTOCHEMICAL STUDY OF TUMOR NECROSIS FACTOR-α, 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)-α, 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. MMP-12 was increased in AMs compared to the control group. The number of AMs with TNF-α and TIMP-2 labeling was higher at 5 days but decreased at 10 days. Short-term CS exposure induced pulmonary inflammation with major participation of MMP-12–positive AMs.