Background An imbalance between proteolytic enzymes\nand their inhibitors is thought to be involved in the pathogenesis\nof chronic obstructive pulmonary disease. Matrix\nmetalloproteinase-1, also known as interstitial collagenase,\nhas been implicated as a potentially important proteinase in\nthe genesis of chronic obstructive pulmonary disease and,\nmore specifically, emphysema.\nMethods We performed quantitative immunohistochemical\nassessment of matrix metalloproteinase-1 expression in\nthe resected lung of 20 smokers/ex-smokers who had varying\nseverity of airflow obstruction and emphysema and\ncompared this with the lungs of 5 nonsmokers. Emphysema\nwas measured using a morphometric measure of the lungs�\nsurface area/volume ratio and with qualitative and quantitative\ncomputed tomography (CT) measures of emphysema.\nResults There were significantly more matrix metalloproteinase-\n1-expressing alveolar macrophages and type II\npneumocytes as well as a greater percentage of small airways\nthat stained positively for matrix metalloproteinase-1\nin the lungs of smokers than in those of nonsmokers\n(p\\0.0001, p\\0.0001, and p = 0.0003, respectively).\nThe extent of staining of type II pneumocytes and airways\nfor matrix metalloproteinase-1 was significantly related to\nthe extent of smoking (p = 0.012 and p = 0.013, respectively).\nIn addition, the extent of matrix metalloproteinase-\n1 staining of alveolar macrophages was related to the lung\nsurface area/volume ratio and to qualitative estimates of\nemphysema on CT.\nConclusion These findings suggest that cigarette smoking\nincreases expression of matrix metalloproteinase-1 in\nalveolar macrophages as well as in alveolar and small\nairway epithelial cells. Smokers who develop emphysema\nhave increased alveolar macrophage expression of matrix\nmetalloproteinase-1.
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