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    Tissue plasminogen activator potently stimulates pleural effusion via a monocyte chemotactic protein-1-dependent mechanism

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    Authors
    Lansley, S.
    Cheah, H.
    Della Vergiliana, J.
    Chakera, Aron
    Lee, Y.
    Date
    2015
    Type
    Journal Article
    
    Metadata
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    Citation
    Lansley, S. and Cheah, H. and Della Vergiliana, J. and Chakera, A. and Lee, Y. 2015. Tissue plasminogen activator potently stimulates pleural effusion via a monocyte chemotactic protein-1-dependent mechanism. American Journal of Respiratory Cell and Molecular Biology. 53 (1): pp. 105-112.
    Source Title
    American Journal of Respiratory Cell and Molecular Biology
    DOI
    10.1165/rcmb.2014-0017OC
    ISSN
    1044-1549
    School
    Curtin Medical School
    URI
    http://hdl.handle.net/20.500.11937/7694
    Collection
    • Curtin Research Publications
    Abstract

    Copyright © 2015 by the American Thoracic Society. Pleural infection is common. Evacuation of infected pleural fluid is essential for successful treatment, but it is often difficult because of adhesions/loculations within the effusion and the viscosity of the fluid. Intrapleural delivery of tissue plasminogen activator (tPA) (to break the adhesions) and deoxyribonuclease (DNase) (to reduce fluid viscosity) has recently been shown to improve clinical outcomes in a large randomized study of pleural infection. Clinical studies of intrapleural fibrinolytic therapy have consistently shown subsequent production of large effusions, the mechanism(s) of which are unknown. We aimed to determine the mechanism by which tPA induces exudative fluid formation. Intrapleural tPA, with or without DNase, significantly induced pleural fluid accumulation in CD1 mice (tPA alone: median [interquartile range], 53.5 [30-355] µl) compared with DNase alone or vehicle controls (both, 0.0 [0.0-0.0] µl) after 6 hours. Fluid induction was reproduced after intrapleural delivery of streptokinase and urokinase, indicating a class effect. Pleural fluid monocyte chemotactic protein (MCP)-1 levels strongly correlated with effusion volume (r = 0.7302; P = 0.003), and were significantly higher than MCP-1 levels in corresponding sera. Mice treated with anti-MCP-1 antibody (P < 0.0001) or MCP-1 receptor antagonist (P = 0.0049) demonstrated a significant decrease in tPA-induced pleural fluid formation (by up to 85%). Our data implicate MCP-1 as the key molecule governing tPA-induced fluid accumulation. The role of MCP-1 in the development of other exudative effusions warrants examination.

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