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dc.contributor.authorW. Joost Wiersingaen_US
dc.contributor.authorLiesbeth M. Kageren_US
dc.contributor.authorJoppe W.R. Hoviusen_US
dc.contributor.authorGerritje J.W. Van Der Windten_US
dc.contributor.authorAlex F. De Vosen_US
dc.contributor.authorJoost C.M. Meijersen_US
dc.contributor.authorJoris J. Roelofsen_US
dc.contributor.authorArjen Dondorpen_US
dc.contributor.authorMarcel Levien_US
dc.contributor.authorNicholas P. Dayen_US
dc.contributor.authorSharon J. Peacocken_US
dc.contributor.authorTom Van Der Pollen_US
dc.contributor.otherAcademic Medical Centre, University of Amsterdamen_US
dc.contributor.otherMahidol Universityen_US
dc.contributor.otherNuffield Department of Clinical Medicineen_US
dc.date.accessioned2018-09-24T09:06:59Z-
dc.date.available2018-09-24T09:06:59Z-
dc.date.issued2010-03-15en_US
dc.identifier.citationJournal of Immunology. Vol.184, No.6 (2010), 3079-3086en_US
dc.identifier.issn15506606en_US
dc.identifier.issn00221767en_US
dc.identifier.other2-s2.0-77951918695en_US
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=77951918695&origin=inwarden_US
dc.identifier.urihttp://repository.li.mahidol.ac.th/dspace/handle/123456789/29250-
dc.description.abstractUrokinase 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.en_US
dc.rightsMahidol Universityen_US
dc.source.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=77951918695&origin=inwarden_US
dc.subjectImmunology and Microbiologyen_US
dc.titleUrokinase receptor is necessary for bacterial defense against pneumonia-derived septic melioidosis by facilitating phagocytosisen_US
dc.typeArticleen_US
dc.rights.holderSCOPUSen_US
dc.identifier.doi10.4049/jimmunol.0901008en_US
Appears in Collections:Scopus 2006-2010

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