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Thromb Haemost 1998; 79(03): 649-655
DOI: 10.1055/s-0037-1614961
Review Articles
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Tissue Factor Pathway Inhibitor in Tetracycline-induced Pleuritis in Rabbits

Steven Idell
1   From the Departments of Specialty Care Services, Pathology and Biochemistry, The University of Texas Health Center at Tyler, Tyler TX, USA
,
Usha Pendurthi
1   From the Departments of Specialty Care Services, Pathology and Biochemistry, The University of Texas Health Center at Tyler, Tyler TX, USA
,
Siegfried Pueblitz
1   From the Departments of Specialty Care Services, Pathology and Biochemistry, The University of Texas Health Center at Tyler, Tyler TX, USA
,
Kathleen Koenig
1   From the Departments of Specialty Care Services, Pathology and Biochemistry, The University of Texas Health Center at Tyler, Tyler TX, USA
,
Todd Williams
1   From the Departments of Specialty Care Services, Pathology and Biochemistry, The University of Texas Health Center at Tyler, Tyler TX, USA
,
Vijay Mohan L. Rao
1   From the Departments of Specialty Care Services, Pathology and Biochemistry, The University of Texas Health Center at Tyler, Tyler TX, USA
› Author AffiliationsSupport: NIH HL45018 (SI) and NIH HL42813 (LVMR), The RGK Foundation, The Gina Sabatasse and Cindy Armstrong Brown Research Grant Awards and The Temple Chair in Idiopathic Pulmonary Fibrosis (SI). During this investigation, LVMR was the recipient of a Research Career Development Award (HL 02590) from the NIH.
Further Information

Publication History

Received 11 September 1997

Accepted after revision 29 October 1997

Publication Date:
07 December 2017 (online)

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Summary

Pleural fibrin deposition that promotes loculation and fibrosis after pleural injury is initiated by tissue factor (TF). In this study, we sought to determine if tissue factor pathway inhibitor (TFPI), an inhibitor of the TF-factor VIIa complex, was likewise expressed in tetracycline (TCN)-induced pleural injury and, if so, whether TFPI was locally elaborated. Pleural fluid TFPI activity approximated that of plasma by 24 h and doubled by 3 days after intrapleural TCN. By contrast, pleural fluid coagulation factors VII and V remained below plasma concentrations at these intervals. Immunohistochemical studies demonstrated TF, TFPI and fibrin localized in pleural and subpleural tissues and within intrapleural adhesions. TFPI activity and mRNA were also elaborated by rabbit pleural mesothelial cells and lung fibroblasts. TFPI is locally expressed and pleural fluid TFPI exceeds plasma levels during TCN-induced pleural injury. Resident cells as well as extravasation likely contribute to intrapleural TFPI. TFPI expression temporally and anatomically approximates that of TF and may limit TF-induced fibrin deposition in evolving TCN-induced pleuritis.

 

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