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Blood, 1 June 2006, Vol. 107, No. 11, pp. 4399-4406. Prepublished online as a Blood First Edition Paper on February 7, 2006; DOI 10.1182/blood-2005-09-3776. This Article Full Text (PDF) All Versions of this Article: 2005-09-3776v1 107/11/4399    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 Fujimi, S. Articles by Lapchak, P. H Search for Related Content PubMed PubMed Citation Articles by Fujimi, S. Articles by Lapchak, P. H Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted September 20, 2005 Accepted January 26, 2006 Platelet depletion in mice increases mortality after thermal injury Satoshi Fujimi, Malcolm P MacConmara, Adrian A Maung, Yan Zang, John A Mannick, James A Lederer, and Peter H Lapchak* Julian and Eunice Cohen Laboratory for Surgical Research, Department of Surgery, Immunology, Brigham and Women's Hospital, and Harvard Medical School,, Boston, Massachusetts, USA Department of Surgery, Massachusetts General Hospital, Boston, Massachusetts, USA Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas, USA * Corresponding author; email: plapchak{at}partners.org. Platelets play a fundamental role in maintaining hemostasis and have been shown to participate in innate and adaptive immunity. However, the role of platelets in the immune response to injury remains undefined. We tested the importance of platelets in the host response to serious injury in a newly developed platelet-deficient mouse model. Wild type and platelet-depleted C57BL/6J mice underwent a 25% full thickness total body surface area thermal- or sham-injury. Platelet-deficient mice showed survival of 51% at 48 hours after injury compared to 94-100% survival in experimental control mice (P<.0001). Necropsy and histology ruled out hemorrhage and hypovolemia as causes of death. Percentages of peripheral blood monocytes (P<.01) and neutrophils (P<.05) were increased between 36-48 hours after thermal injury in platelet-deficient mice compared to control mice. Plasma levels of TNF (P<.0001), IL-6 (P<.001), and MCP-1 (P<.05) were also elevated by 24 hours while levels of TGF1 were reduced between 24-36 hours following injury in platelet-depleted mice (P<.001) compared to control mice. Our findings demonstrate for the first time that platelets play a critical protective role during the host response to injury. Moreover, our findings suggest that platelets, and more importantly, platelet-derived TGF1, modulate the systemic inflammatory response occurring after injury. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. W. S. Sio, M. K. Puthia, J. Lu, S. Moochhala, and M. Bhatia The Neuropeptide Substance P Is a Critical Mediator of Burn-Induced Acute Lung Injury J. Immunol., June 15, 2008; 180(12): 8333 - 8341. [Abstract] [Full Text] [PDF] M. Collin, O. Shannon, and L. Bjorck From the Cover: IgG glycan hydrolysis by a bacterial enzyme as a therapy against autoimmune conditions PNAS, March 18, 2008; 105(11): 4265 - 4270. [Abstract] [Full Text] [PDF]

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