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Expression of matrix metalloproteinases in pigs with hyperoxia-induced acute lung injury

First Dept of Internal Medicine, Kumamoto University School of Medicine, Kumamoto, Japan

CORRESPONDENCE: M. Suga, First Dept of Internal Medicine, Kumamoto University School of Medicine, 1-;1-;1 Honjo, Kumamoto, 860-0811, Japan. Fax: 81 963710582

Keywords: acute lung injury, elastase, hyperoxia, matrix metalloproteinases

Received: July 18, 2000
Accepted May 28, 2001

This work was supported by a grant-in-aid for interstitial lung diseases from the Japanese Ministry of Health and Welfare, and a grant-in-aid for scientific research 12670565 from the Japanese Ministry of Education, Culture, Sports, Science and Technology.

The aim of this study was to determine the role of matrix metalloproteinases (MMPs) in the pathogenesis of acute lung injury induced by hyperoxia.

Twenty-three pigs were exposed in sealed cages to >80% oxygen (for 24–120 h) or room air. Correlation between MMP-;2/MMP-;9 activity, measured by gelatin zymography in bronchoalveolar lavage fluid (BALF), and the histological findings and pathological parameters were examined in detail. Sources of these MMPs in the hyperoxic lung were analysed by immunohistochemistry.

The histological progression of acute lung injury in this model ranged from the early exudative to the early proliferative phase of diffuse alveolar damage (DAD). MMP-;2 and -;9 activities were elevated under prolonged hyperoxic exposure. MMP-;9 activity correlated significantly with the oxygen tension in arterial blood/inspiratory oxygen fraction, the lung wet-to-dry weight ratio, and the number of neutrophils in BALF, whereas MMP-;2 activity did not correlate at all with these factors. MMP-;9 activity correlated more closely with the pathological findings of DAD than did MMP-;2 activity. Strong MMP-;9 expression was observed in neutrophils, alveolar macrophages as well as alveolar lining epithelial cells.

These results suggest that matrix metalloproteinase, which may derive from neutrophils recruited into airspaces, plays an important role in the pathogenesis of hyperoxic diffuse alveolar damage.

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