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Inhibiting interleukin-1 and tumor necrosis factor-alpha does not reduce
induction of plasminogen activator inhibitor type-1 by endotoxin in rats in
vivo
JJ Emeis, R Hoekzema and AF de Vos
Gaubius Laboratory TNO-PG, Leiden, The Netherlands.
In experimental animals and humans, intravenous (i.v.) injection of
endotoxin induces large increases in circulating plasminogen activator
inhibitor type-1 (PAI-1), a major inhibitor of blood fibrinolysis. A
similar increase is seen after the injection of interleukin-1 (IL-1) or of
tumor necrosis factor-alpha (TNF-alpha), suggesting that these cytokines
mediate the induction, by endotoxin, of PAI-1. To test this hypothesis we
pretreated rats, before i.v. endotoxin, with compounds that inhibit the
formation of cytokines (pentoxifylline; dexamethasone), or with compounds
that inhibit the action of these cytokines (anti-TNF antiserum for
TNF-alpha; IL-1 receptor antagonist for IL-1). None of these pretreatments
affected the induction of PAI-1 synthesis by endotoxin. However,
pretreatment did reduce the endotoxin- induced increase in plasma tPA
antigen concentration. Thus, the data suggest that, in rats in vivo,
TNF-alpha and IL-1 are not significantly involved in the induction of PAI-1
by endotoxin.
Volume 85,
Issue 1,
pp. 115-120,
01/01/1995
Copyright © 1995 by The American Society of Hematology
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