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Published ahead of print on February 20, 2003, doi:10.1164/rccm.200208-905OC
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American Journal of Respiratory and Critical Care Medicine Vol 167. pp. 1687-1694, (2003)
© 2003 American Thoracic Society

Original Article

Thrombin-activatable Fibrinolysis Inhibitor and Protein C Inhibitor in Interstitial Lung Disease

Hajime Fujimoto, Esteban Cesar Gabazza, Osamu Hataji, Hisamichi Yuda, Corina Nayade D'Alessandro-Gabazza, Mariko Nakano, Omar Enrique Franco, Tatsuya Hayashi, Koji Suzuki, Yukihiko Adachi and Osamu Taguchi

Respiratory Division of the Third Department of Internal Medicine; Department of Molecular Pathobiology; and Department of Urology, Mie University School of Medicine, Tsu, Mie, Japan

Correspondence and requests for reprints should be addressed to Esteban C. Gabazza, Third Department of Internal Medicine, Respiratory Division, Mie University School of Medicine, Edobashi 2–174, Tsu City, Mie 514–8507, Japan. E-mail: gabazza{at}clin.medic.mie-u.ac.jp

Intraalveolar activation of the coagulation system due to reduced fibrinolytic function plays a critical role in the pathogenesis of interstitial lung disease. Recently, a new potent inhibitor of fibrinolysis, thrombin-activatable fibrinolysis inhibitor, has been isolated and characterized from human plasma. This study evaluated the levels of thrombin-activatable fibrinolysis inhibitor and protein C inhibitor, another suppressor of fibrinolysis, in the bronchoalveolar lavage fluid from patients with interstitial lung disease. There were 82 patients with interstitial lung disease and 8 normal subjects. The bronchoalveolar lavage fluid levels of thrombin-activatable fibrinolysis inhibitor and protein C inhibitor were significantly higher in all patients with interstitial lung disease than in normal subjects. Both inhibitors of fibrinolysis were significantly and inversely correlated with fibrinolytic activity in all patients. The levels of thrombin-activatable fibrinolysis inhibitor were significantly correlated with those of protein C inhibitor, thrombin–antithrombin complex, and monocyte chemoattractant protein-1. Reverse transcriptase-polymerase chain reaction showed that alveolar macrophages isolated from patients with interstitial lung disease as well as immortalized lung epithelial cell lines express thrombin-activatable fibrinolysis inhibitor antigen. Overall, these findings suggest that thrombin-activatable fibrinolysis inhibitor and protein C inhibitor may play important roles in the mechanism of intraalveolar hypofibrinolysis associated with interstitial lung diseases.

Key Words: lung fibrosis • plasmin • coagulation • activated protein C • metalloproteinases




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