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Infection and Immunity, April 2000, p. 2156-2160, Vol. 68, No. 4
Laboratory of Experimental Internal Medicine,
Academic Medical Center, University of Amsterdam, Amsterdam, The
Netherlands
Received 27 August 1999/Accepted 10 January 2000
The receptor for urokinase-type plasminogen activator (uPAR) (CD87)
plays an important role in leukocyte adhesion and migration. To assess
the effect of endotoxin on cellular uPAR, uPAR expression was
determined on leukocytes by fluorescence-activated cell sorter analysis
in seven healthy subjects following intravenous injection of endotoxin
(lot G; 4 ng/kg). Endotoxin induced a transient increase in uPAR
expression on monocytes, reaching a 92% ± 46% increase over baseline
expression after 6 h (P < 0.05). Endotoxin
did not influence uPAR expression on granulocytes, while uPAR remained undetectable on lymphocytes. Endotoxin also increased soluble uPAR
levels in plasma (P < 0.05). Stimulation of human
whole blood with endotoxin or gram-positive stimuli in vitro also
resulted in an upregulation of monocyte uPAR expression. Although tumor necrosis factor alpha (TNF) upregulated monocyte uPAR expression, anti-TNF did not influence the endotoxin-induced increase in monocyte uPAR expression. These data suggest that infectious stimuli may influence monocyte function in vivo by enhancing the expression of uPAR.
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Copyright © 2000, American Society for Microbiology. All rights reserved.
Upregulation of Monocyte Urokinase Plasminogen
Activator Receptor during Human Endotoxemia
*
Corresponding author. Mailing address: Laboratory of
Experimental Internal Medicine, Rm. G2-105, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands. Phone: 31-20-5666034. Fax: 31-20-6977192. E-mail: P.E.Dekkers{at}AMC.UVA.NL.
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