Medical Journals

Platelet Depletion in Mice Increases Mortality After Thermal Injury.

Authors:
  • Fujimi Satoshi
  • MacConmara Malcolm P
  • Maung Adrian A
  • Zang Yan
  • Mannick John A
  • Lederer James A
  • Lapchak Peter H

From: Julian and Eunice Cohen Laboratory for Surgical Research, Department of Surgery, Brigham and Women’s Hospital, Boston, MA 02115, USA.

Blood

  • Publish Date: Jun 2006
  • ISSN: 0006-4971
  • Volume: 107
  • Issue: 11
  • Pages: 4399-406
  • Medium: Print
  • Language: English
  • Citation (JAMA): Fujimi Satoshi, MacConmara Malcolm P, Maung Adrian A, et al. Platelet Depletion in Mice Increases Mortality After Thermal Injury.. Blood Jun 2006;107:4399-406

Abstract

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 with 94% to 100% survival in experimental control mice (P < .001). 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 and 48 hours after thermal injury in platelet-deficient mice compared with control mice. Plasma levels of TNFalpha (P < .001), IL-6 (P < .001), and MCP-1 (P < .05) were also elevated by 24 hours whereas levels of TGFbeta(1) were reduced between 24 and 36 hours following injury in platelet-depleted mice (P < .001) compared with 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 TGFbeta(1) modulate the systemic inflammatory response occurring after injury.

Mesh Headings (Keywords): Animals, Blood Platelets, Chemokine CCL2, Disease Models, Animal, Heat, Inflammation, Mice, Mice, Inbred C57BL, Platelet Count, Survival Rate, Transforming Growth Factor beta, Tumor Necrosis Factor-alpha, Wounds and Injuries


Check for Full Text / PubMed Unique Identifier (PMID): 16467203


This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.

Linked medical terms appearing on this page are added by Healia to help readers find more information and are not part of the original PubMed document.

The data herein was last updated on July 8th, 2008 and may not reflect the most current and accurate data available from NLM.


Advertisements

About | Privacy Policy | Business Solutions | Advertise | Contact | Add Healia to your site

©2012. Healia / Meredith Corporation  

Use of this site constitutes acceptance of our Terms of Service and Privacy Policy. All content on this Web site, including medical opinion and any other health-related information, is for informational purposes only and should not be used for a specific diagnosis or individual treatment plan for any situation. Use of this site and the information contained herein does not create a doctor-patient relationship. Always seek the direct advice of your doctor in connection with any questions or issues you may have regarding your own health or the health of others.