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Originally published online as doi:10.1189/jlb.0502257 on July 26, 2004

Published online before print July 26, 2004
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(Journal of Leukocyte Biology. 2004;76:571-576.)
© 2004 by Society for Leukocyte Biology

Polymorphonuclear leukocytes from patients with severe sepsis have lost the ability to degrade fibrin via u-PA

E. Moir*, M. Greaves*, G. D. Adey{dagger} and B. Bennett*,1

* Departments of Medicine and Therapeutics, University of Aberdeen, Institute of Medical Science, and
{dagger} Anaesthetics, Grampian Hospitals NHS Trust, Scotland, United Kingdom

1 Correspondence: Department of Medicine and Therapeutics, Institute of Medical Science, Polwarth Building, University of Aberdeen, Foresterhill, Aberdeen AB25 2ZD, Scotland, UK. E-mail: b.bennett{at}abdn.ac.uk

Fibrin persistence in the vasculature is an important complication of sepsis that can often lead to mortality. We have previously established that polymorphonuclear leukocytes (PMN) from healthy individuals have the capacity to degrade fibrin via urokinase-type plaminogen activator (u-PA). We have also demonstrated an increase in u-PA antigen in the plasma of patients suffering from septic shock. In this study, we investigate the hypothesis that PMN from patients with sepsis have lost their fibrinolytic ability and that this might contribute to the persistence of fibrin deposits. We show here that PMN from these patients do not express any u-PA activity, despite retaining some u-PA antigen. Additionally, thrombi prepared from the whole blood of the patients exhibit reduced endogenous lysis compared with those from healthy individuals. These data indicate that loss of fibrinolytic activity from PMN may be a contributing factor in fibrin persistence in the microvasculature in sepsis.

Key Words: fibrinolysis • PMN • urokinase






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