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Published online before print March 1, 2007
Eur Respir J 2007, doi:10.1183/09031936.00097306
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ORIGINAL ARTICLE

Cellular origin of procoagulant and (anti)-fibrinolytic factors in bleomycin-injured lungs

M. Wygrecka 1, P. Markart 2*, C. Ruppert 2, K. Petri 2, K.T. Preissner 1, W. Seeger 2, A. Guenther 2

1 Depts of Biochemistry and
2 Internal Medicine, Faculty of Medicine, University of Giessen Lung Center, Giessen, Germany

* To whom correspondence should be addressed. E-mail: philipp.markart{at}innere.med.uni-giessen.de.


  Abstract

Excessive procoagulant and decreased fibrinolytic activities in the alveolar compartment have been repeatedly documented for inflammatory and fibrotic lung diseases. We determined the contribution of different resident lung cells to the altered local production of components of the coagulation and fibrinolysis systems in bleomycin-injured mouse lungs by cell-specific and quantitative assessment of mRNA levels of various procoagulant and (anti)-fibrinolytic factors.

Laser-assisted microdissection technology was used to sample specific cell populations in combination with subsequent mRNA analysis by real-time quantitative RT-PCR. Additionally, western blot analysis, immunohistochemistry, and activity assays were performed.

Following bleomycin challenge, the strongest induction of tissue factor and plasminogen activator inhibitor (PAI)-1 mRNA expression was observed in alveolar macrophages (approximately 250- and 60-fold induction, respectively). These factors were also upregulated in alveolar type II cells, but to an approximately 6-fold lesser extent. In contrast, PAI-2 expression was induced exclusively in alveolar macrophages. A slight increase of urokinase-type plasminogen activator (uPA) expression was also observed in alveolar macrophages (2-fold induction), however uPA activity was reduced due to disproportionate increase of PAI production.

Alveolar macrophages and, to a lesser extent, alveolar type II cells are the main sources of locally produced procoagulant and anti-fibrinolytic factors in bleomycin-injured lungs.

Keywords:  ALI/ARDS, alveolar macrophage, alveolar type II cell, gene expression and regulation, haemostasis, pulmonary fibrosis




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