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Blood, Vol. 94 No. 7 (October 1), 1999:
pp. 2252-2258
The Effect of a Metalloproteinase Inhibitor (GI5402) on Tumor Necrosis
Factor- (TNF-) and TNF- Receptors During Human Endotoxemia
Pascale E.P. Dekkers,
Fanny N. Lauw,
Tessa ten Hove,
Anje A. te
Velde,
Philip Lumley,
David Becherer,
Sander J.H. van Deventer, and
Tom van der Poll
From the Academic Medical Center, University of Amsterdam, Laboratory
of Experimental Internal Medicine, Amsterdam, the Netherlands;
Department of Clinical Pharmacology, Glaxo Wellcome, Greenford, UK; and
the Department of Biochemistry, Glaxo Wellcome, Research Triangle Park,
NC.
Tumor necrosis factor- (TNF-) is released from the cell
surface by cleavage of pro-TNF- by metalloproteinases (MPs). In cell cultures, inhibition of MPs has been found not only to reduce the
release of TNF-, but also to enhance the surface expression of
TNF- and TNF- receptors, which might lead to a proinflammatory effect. To determine the effect of MP inhibition during inflammation in
humans, 7 healthy subjects were studied after intravenous injection of
lipopolysaccharide (LPS; 4 ng/kg) preceded ( 20
minutes) by an oral dose of the MP inhibitor GI5402 (100 mg) or
matching placebo. GI5402 strongly reduced LPS-induced TNF- release
(P < .001), but did not influence the increase in
monocyte-bound TNF-. In addition, GI5402 attenuated the rise in
plasma-soluble TNF- receptors types I and II after LPS injection
(both P < .001), but did not change the LPS-induced decreases
in granulocyte and monocyte TNF- receptor expression. These data
suggest that MP inhibitors may be useful as a treatment modality in
diseases in which excessive production of TNF- is considered to play
an important role. Furthermore, unlike in vitro, no evidence has been
found in vivo with MP inhibition for a potential proinflammatory effect
due to increases in membrane-bound TNF- and TNF- receptor number.
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