Tissue Factor Pathway Inhibitor in Tetracycline-induced Pleuritis in Rabbits

Steven Idell; Usha Pendurthi; Siegfried Pueblitz; Kathleen Koenig; Todd Williams; Vijay Mohan L. Rao

doi:10.1055/s-0037-1614961

Thrombosis and Haemostasis, Table of Contents

Thromb Haemost 1998; 79(03): 649-655
DOI: 10.1055/s-0037-1614961

Review Articles

Schattauer GmbH

Tissue Factor Pathway Inhibitor in Tetracycline-induced Pleuritis in Rabbits

Steven Idell

¹From the Departments of Specialty Care Services, Pathology and Biochemistry, The University of Texas Health Center at Tyler, Tyler TX, USA

,

Usha Pendurthi

¹From the Departments of Specialty Care Services, Pathology and Biochemistry, The University of Texas Health Center at Tyler, Tyler TX, USA

,

Siegfried Pueblitz

¹From the Departments of Specialty Care Services, Pathology and Biochemistry, The University of Texas Health Center at Tyler, Tyler TX, USA

,

Kathleen Koenig

¹From the Departments of Specialty Care Services, Pathology and Biochemistry, The University of Texas Health Center at Tyler, Tyler TX, USA

,

Todd Williams

¹From the Departments of Specialty Care Services, Pathology and Biochemistry, The University of Texas Health Center at Tyler, Tyler TX, USA

,

Vijay Mohan L. Rao

¹From the Departments of Specialty Care Services, Pathology and Biochemistry, The University of Texas Health Center at Tyler, Tyler TX, USA

› Author Affiliations

Abstract

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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References

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