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Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/29250
Title: Urokinase receptor is necessary for bacterial defense against pneumonia-derived septic melioidosis by facilitating phagocytosis
Authors: W. Joost Wiersinga
Liesbeth M. Kager
Joppe W.R. Hovius
Gerritje J.W. Van Der Windt
Alex F. De Vos
Joost C.M. Meijers
Joris J. Roelofs
Arjen Dondorp
Marcel Levi
Nicholas P. Day
Sharon J. Peacock
Tom Van Der Poll
Academic Medical Centre, University of Amsterdam
Mahidol University
Nuffield Department of Clinical Medicine
Keywords: Immunology and Microbiology
Issue Date: 15-Mar-2010
Citation: Journal of Immunology. Vol.184, No.6 (2010), 3079-3086
Abstract: Urokinase receptor (urokinase-type plasminogen activator receptor [uPAR], CD87), a GPI-anchored protein, is considered to play an important role in inflammation and fibrinolysis. The Gram-negative bacterium Burkholderia pseudomallei is able to survive and replicate within leukocytes and causes melioidosis, an important cause of pneumonia-derived community-acquired sepsis in Southeast Asia. In this study, we investigated the expression and function of uPAR both in patients with septic melioidosis and in a murine model of experimental melioidosis. uPAR mRNA and surface expression was increased in patients with septic melioidosis in/on both peripheral blood monocytes and granulocytes as well as in the pulmonary compartment during experimental pneumonia-derived melioidosis in mice. uPAR-deficient mice intranasally infected with B. pseudomallei showed an enhanced growth and dissemination of B. pseudomallei when compared with wild-type mice, corresponding with increased pulmonary and hepatic inflammation. uPAR knockout mice demonstrated significantly reduced neutrophil migration toward the pulmonary compartment after inoculation with B. pseudomallei. Further in vitro experiments showed that uPAR-deficient macrophages and granulocytes display a markedly impaired phagocytosis of B. pseudomallei. Additional studies showed that uPAR deficiency did not influence hemostatic and fibrinolytic responses during severe melioidosis. These data suggest that uPAR is crucially involved in the host defense against sepsis caused by B. pseudomallei by facilitating the migration of neutrophils toward the primary site of infection and subsequently facilitating the phagocytosis of B. pseudomallei. Copyright © 2010 by The American Association of Immunologists, Inc.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=77951918695&origin=inward
http://repository.li.mahidol.ac.th/dspace/handle/123456789/29250
ISSN: 15506606
00221767
Appears in Collections:Scopus 2006-2010

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