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Effect of canine hyperimmune plasma on TNFα and inflammatory cell levels in a lipopolysaccharide-mediated rat air pouch model of inflammation

Authors
Journal
Critical Care
1364-8535
Publisher
Springer (Biomed Central Ltd.)
Publication Date
Volume
13
Identifiers
DOI: 10.1186/cc8064
Keywords
  • Poster Presentation
Disciplines
  • Biology

Abstract

Typeset abstracts.qxd S1 Available online http://ccforum.com/supplements/13/S4 Critical Care Volume 13 Suppl 4, 2009 Sepsis 2009 Amsterdam, the Netherlands, 11–14 November 2009 Published online: 11 November 2009 These abstracts are available online at http://ccforum.com/supplements/13/S4 © 2009 BioMed Central Ltd P1 Urokinase receptor is necessary for bacterial defense against Gram-negative sepsis (melioidosis) by facilitating phagoctytosis W Joost Wiersinga1,2, JWR Hovius1,2, GJW van der Windt1,2, JCM Meijers3, JJ Roelofs4, A Dondorp5, M Levi1, NP Day5,6, SJ Peacock5,6, T van der Poll1,2 1Center for Infection and Immunity Amsterdam, 2Center for Experimental and Molecular Medicine, 3Department of Vascular Medicine and 4Department of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands; 5Mahidol-Oxford Tropical Medicine Research Unit, Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand; 6Center for Clinical Vaccinology and Tropical Medicine, Nuffield Department of Clinical Medicine, University of Oxford, UK Critical Care 2009, 13(Suppl 4):P1 (doi: 10.1186/cc8057) Introduction Urokinase receptor (uPAR, CD87), a glycosylphos- phatidylinositol-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 South- east Asia. We here investigated the expression and function of uPAR both in patients with septic melioidosis and in a murine model of experimental melioidosis. Methods Using a translational approach we conducted a patient study in patients with culture-confirmed sepsis caused by B. pseudomallei, in vitro experiments using wild-type (WT) and uPAR knockout (KO) cells, and mouse studies using WT and uPAR KO mice inoculated with B. pseudomallei. Results uPAR mRNA and surface expression was increased in p

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