Upregulation of Monocyte Urokinase Plasminogen Activator Receptor during Human Endotoxemia

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Published in:Infection and Immunity Vol. 68; no. 4; pp. 2156 - 2160
Main Authors: DEKKERS, P. E. P, TEN HOVE, T, TE VELDE, A. A, VAN DEVENTER, S. J. H, VAN DER POLL, T
Format: Journal Article
Language:English
Published: Washington, DC American Society for Microbiology 01-04-2000
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Abstract Classifications Services IAI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue IAI About IAI Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy Connect to IAI IAI RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0019-9567 Online ISSN: 1098-5522 Copyright © 2014 by the American Society for Microbiology.   For an alternate route to IAI .asm.org, visit: IAI       
AbstractList 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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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% plus or minus 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.
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.
Author Anje A. te Velde
Pascale E. P. Dekkers
Tessa ten Hove
Tom van der Poll
Sander J. H. van Deventer
AuthorAffiliation Laboratory of Experimental Internal Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
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  givenname: S. J. H
  surname: VAN DEVENTER
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Issue 4
Keywords Human
u-Plasminogen activator
Serine endopeptidases
Monocyte
Enzyme
Escherichia coli
Host agent relation
Stimulation
Gene expression
Endotoxin
In vitro
Biological activity
Peptidases
Regulation(control)
Lipopolysaccharide
Bacteria
Hydrolases
Models
Endotoxemia
Enterobacteriaceae
Biological receptor
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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@AMC.UVA.NL.
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SSID ssj0014448
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The receptor for urokinase-type plasminogen activator (uPAR) (CD87) plays an important role in leukocyte adhesion and migration. To assess the effect of...
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StartPage 2156
SubjectTerms Adult
Bacteriology
Biological and medical sciences
Blood Cell Count
Dose-Response Relationship, Drug
Endotoxemia - chemically induced
Endotoxemia - enzymology
Enzyme Precursors - blood
Flow Cytometry
Fundamental and applied biological sciences. Psychology
Host Response and Inflammation
Humans
Injections, Intravenous
Leukocytes - enzymology
Lipopolysaccharides
Lipopolysaccharides - administration & dosage
Lipopolysaccharides - pharmacology
Male
Microbiology
Monocytes - enzymology
Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains
Receptors, Cell Surface - blood
Receptors, Urokinase Plasminogen Activator
Time Factors
Tumor Necrosis Factor-alpha - physiology
u-Plasminogen activator receptors
Up-Regulation
Title Upregulation of Monocyte Urokinase Plasminogen Activator Receptor during Human Endotoxemia
URI http://iai.asm.org/content/68/4/2156.abstract
https://www.ncbi.nlm.nih.gov/pubmed/10722614
https://search.proquest.com/docview/17516420
https://pubmed.ncbi.nlm.nih.gov/PMC97398
Volume 68
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