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Interleukin-10 inhibits activation of coagulation and fibrinolysis during
human endotoxemia
D Pajkrt, T van der Poll, M Levi, DL Cutler, MB Affrime, A van den Ende, JW ten Cate and SJ van Deventer
Laboratory of Experimental Internal Medicine and Center for Hemostasis,
Thrombosis, Atherosclerosis and Inflammation Research, Academic Medical
Center, University of Amsterdam, The Netherlands.
Interleukin-10 (IL-10) has been found to inhibit lipopolysaccharide
(LPS)-induced tissue factor expression by monocytes in vitro. To determine
the effects of IL-10 on LPS-induced activation of the hemostatic mechanisms
in vivo, we performed a placebo-controlled, cross- over study of human
endotoxemia. Two groups of eight volunteers were challenged with LPS (4
ng/kg) on two occasions: once in conjunction with placebo, and once with
recombinant human IL-10 (rhIL-10; 25 microg/kg). In group 1, placebo or
rhIL-10 was given 2 minutes before LPS challenge, group 2 received placebo
or rhIL-10 1 hour after LPS administration. Pretreatment with rhIL-10
reduced both LPS-induced activation of the fibrinolytic system (plasma
concentrations of tissue type plasminogen activator,
plasmin-alpha2-antiplasmin complexes, and D- dimer), and inhibition of
fibrinolysis (plasma levels of plasminogen activator inhibitor 1), whereas
posttreatment only inhibited the latter response. Both IL-10 pre- and
posttreatment attenuated activation of the coagulation system (plasma
levels of prothrombin fragment F1 + 2 and thrombin-antithrombin complexes).
These results indicate that rhIL- 10, besides its well-described inhibitory
effects on cytokine release, potently modulates the fibrinolytic system and
inhibits the coagulant responses during endotoxemia.
Volume 89,
Issue 8,
pp. 2701-2705,
04/15/1997
Copyright © 1997 by The American Society of Hematology
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