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Prepublished online as a Blood First Edition Paper on July 10, 2003; DOI 10.1182/blood-2003-02-0426. This Article Full Text (PDF) All Versions of this Article: 2003-02-0426v1 102/8/2843    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Alugupalli, K. R Articles by Leong, J. M Search for Related Content PubMed PubMed Citation Articles by Alugupalli, K. R Articles by Leong, J. M Social Bookmarking                   What's this? Submitted February 7, 2003 Accepted June 26, 2003 Spirochete-platelet attachment and thrombocytopenia in murine relapsing fever Borreliosis Kishore R Alugupalli, Alan D Michelson, Isabelle Joris, Tom G Schwan, Kairbaan Hodivala-Dilke, Richard O Hynes, and John M Leong* Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, Worcester, MA, USA Department of Pediatrics, University of Massachusetts Medical School, Worcester, MA, USA Department of Pathology, University of Massachusetts Medical School, Worcester, MA, USA Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, Hamilton, MT, USA Howard Hughes Medical Institute, Chevy Chase, MD, USA Department of Biology, Massachusetts Institute of Technology, Cambridge, MA, USA * Corresponding author; email: john.leong{at}umassmed.edu. Thrombocytopenia is common in individuals infected with relapsing fever Borreliae. We previously showed that the relapsing fever spirochete Borrelia hermsii binds to and activates human platelets in vitro, and that after platelet activation, high-level spirochete-platelet attachment is mediated by integrin IIb3, a receptor that requires platelet activation for full function. Here we established that B. hermsii infection of the mouse results in severe thrombocytopenia and a functional defect in hemostasis due to accelerated platelet loss. Disseminated intravascular coagulation, immune thrombocytopenic purpura or splenic sequestration did not play a discernable role in this model. Instead, spirochete-platelet complexes were detected in the blood of infected mice, suggesting that platelet attachment by bacteria might result in platelet clearance. Consistent with this, splenomegaly and thrombocytopenia temporally correlated with spirochetemia, and the severity of thrombocytopenia directly correlated with the degree of spirochetemia. Activation of platelets and integrin IIb3 were apparently not required for either bacterium-platelet binding or for platelet clearance, because the bacterium-bound platelets in the circulation were not activated, and platelet binding and thrombocytopenia during infection of 3-deficient and wild type mice were indistinguishable. These findings suggest that thrombocytopenia of relapsing fever is the result of platelet clearance after b3-independent bacterial attachment to circulating platelets. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: K. C. MacNamara, R. Racine, M. Chatterjee, D. Borjesson, and G. M. Winslow Diminished Hematopoietic Activity Associated with Alterations in Innate and Adaptive Immunity in a Mouse Model of Human Monocytic Ehrlichiosis Infect. Immun., September 1, 2009; 77(9): 4061 - 4069. [Abstract] [Full Text] [PDF] J. E. Lopez, S. F. Porcella, M. E. Schrumpf, S. J. Raffel, C. H. 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