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1 Dept of Medicine and Therapeutics, University College Dublin, Ireland. 2 Faculty of Medicine and Biomedicine and 3 Dept of Clinical Veterinary Medicine, Faculty of Veterinary Medicine, University of Helsinki, Finland. 4 Institute of Experimental and Clinical Medicine, Tallinn, Estonia
CORRESPONDENCE: M.T. Henry, Dept of Respiratory Medicine, Leeds General Infirmary, Great George Street, Leeds, LS1 3EX, UK. Fax: 44 1133926316. E-mail: Michael.Henry@leedsth.nhs.uk
Keywords: collagenases, idiopathic pulmonary fibrosis, matrix metalloproteinases, tissue inhibitor of metalloproteinase-1, sarcoidosis
Received: March 19, 2002
Accepted July 16, 2002
This work was supported by the EU Grant BMH4-CT96-0152 as part of the Biomed 2 EUROLUNG consortium.
The purpose of this study was to examine the role of interstitial collagenases, members of the family of matrix metalloproteinases, in the development of pulmonary fibrosis.
The activity, levels and molecular forms of collagenases (matrix metalloproteinases (MMP)-1, -8 and -13), gelatinase B (MMP-9) and its main endogenous inhibitor, tissue inhibitor of metalloproteinase-1 (TIMP-1) were assessed in bronchoalveolar lavage fluid (BALF) from patients with idiopathic pulmonary fibrosis (IPF) and sarcoidosis patients with varying degrees of pulmonary parenchymal involvement.
Collagenase activity was elevated in IPF and group 3 sarcoidosis patients. A positive correlation between BALF collagenase activity and MMP-8 levels was also observed. Western immunoblotting revealed the presence of two isoforms of MMP-8 in patient samples; an 80 kD form representing latent enzyme from polymorphonuclear neutrophils and a 55 kD form representing the fibroblast-type proform. MMP-9 levels were also elevated in both IPF and group 3 sarcoidosis patients, while TIMP-1 levels remained normal, indicating a shift in the balance between the enzyme and inhibitor, favouring MMP-9.
Matrix metalloproteinase-8 is the major contributor to the bronchoalveolar lavage fluid collagenase activity in the airways of patients with idiopathic pulmonary fibrosis and sarcoidosis and may initiate collagen destruction and remodelling leading to the development of pulmonary fibrosis.
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