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 |
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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. 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 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 |
AuthorAffiliation_xml | – name: Laboratory of Experimental Internal Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands |
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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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Notes | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 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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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 |
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