Get access

Distinct roles of trauma and transfusion in induction of immune modulation after injury

Authors

  • Rachael P. Jackman,

    Corresponding author
    1. From the Blood Systems Research Institute, San Francisco, California; the Departments of Surgery and Political Science, University of California, Davis, California; the Departments of Laboratory Medicine and Medicine, University of California, San Francisco, California; and the Division of Epidemiology, School of Public Health, University of California, Berkeley, California.
    Search for more papers by this author
  • Garth H. Utter,

    1. From the Blood Systems Research Institute, San Francisco, California; the Departments of Surgery and Political Science, University of California, Davis, California; the Departments of Laboratory Medicine and Medicine, University of California, San Francisco, California; and the Division of Epidemiology, School of Public Health, University of California, Berkeley, California.
    Search for more papers by this author
  • Marcus O. Muench,

    1. From the Blood Systems Research Institute, San Francisco, California; the Departments of Surgery and Political Science, University of California, Davis, California; the Departments of Laboratory Medicine and Medicine, University of California, San Francisco, California; and the Division of Epidemiology, School of Public Health, University of California, Berkeley, California.
    Search for more papers by this author
  • John W. Heitman,

    1. From the Blood Systems Research Institute, San Francisco, California; the Departments of Surgery and Political Science, University of California, Davis, California; the Departments of Laboratory Medicine and Medicine, University of California, San Francisco, California; and the Division of Epidemiology, School of Public Health, University of California, Berkeley, California.
    Search for more papers by this author
  • Matthew M. Munz,

    1. From the Blood Systems Research Institute, San Francisco, California; the Departments of Surgery and Political Science, University of California, Davis, California; the Departments of Laboratory Medicine and Medicine, University of California, San Francisco, California; and the Division of Epidemiology, School of Public Health, University of California, Berkeley, California.
    Search for more papers by this author
  • Robert W. Jackman,

    1. From the Blood Systems Research Institute, San Francisco, California; the Departments of Surgery and Political Science, University of California, Davis, California; the Departments of Laboratory Medicine and Medicine, University of California, San Francisco, California; and the Division of Epidemiology, School of Public Health, University of California, Berkeley, California.
    Search for more papers by this author
  • Hope H. Biswas,

    1. From the Blood Systems Research Institute, San Francisco, California; the Departments of Surgery and Political Science, University of California, Davis, California; the Departments of Laboratory Medicine and Medicine, University of California, San Francisco, California; and the Division of Epidemiology, School of Public Health, University of California, Berkeley, California.
    Search for more papers by this author
  • Ryan M. Rivers,

    1. From the Blood Systems Research Institute, San Francisco, California; the Departments of Surgery and Political Science, University of California, Davis, California; the Departments of Laboratory Medicine and Medicine, University of California, San Francisco, California; and the Division of Epidemiology, School of Public Health, University of California, Berkeley, California.
    Search for more papers by this author
  • Leslie H. Tobler,

    1. From the Blood Systems Research Institute, San Francisco, California; the Departments of Surgery and Political Science, University of California, Davis, California; the Departments of Laboratory Medicine and Medicine, University of California, San Francisco, California; and the Division of Epidemiology, School of Public Health, University of California, Berkeley, California.
    Search for more papers by this author
  • Michael P. Busch,

    1. From the Blood Systems Research Institute, San Francisco, California; the Departments of Surgery and Political Science, University of California, Davis, California; the Departments of Laboratory Medicine and Medicine, University of California, San Francisco, California; and the Division of Epidemiology, School of Public Health, University of California, Berkeley, California.
    Search for more papers by this author
  • Philip J. Norris

    1. From the Blood Systems Research Institute, San Francisco, California; the Departments of Surgery and Political Science, University of California, Davis, California; the Departments of Laboratory Medicine and Medicine, University of California, San Francisco, California; and the Division of Epidemiology, School of Public Health, University of California, Berkeley, California.
    Search for more papers by this author

  • This work was supported by NIH RO1 HL-083388-01A1.

Rachael P. Jackman, Blood Systems Research Institute, 270 Masonic Avenue, San Francisco, CA 94118; e-mail: rjackman@bloodsystems.org.

Abstract

BACKGROUND: Trauma and transfusion can both alter immunity, and while transfusions are common among traumatically injured patients, few studies have examined their combined effects on immunity.

STUDY DESIGN AND METHODS: We tracked the plasma levels of 41 immunomodulatory proteins in 56 trauma patients from time of injury up to 1 year later. In addition, a murine model was developed to distinguish between the effects of transfusion and underlying injury and blood loss.

RESULTS: Thirty-one of the proteins had a significant change over time after traumatic injury, with a mixed early response that was predominantly anti-inflammatory followed by a later increase in proteins involved in wound healing and homeostasis. Results from the murine model revealed similar cytokine responses to humans. In mice, trauma and hemorrhage caused early perturbations in a number of the pro- and anti-inflammatory mediators measured, and transfusion blunted early elevations in interleukin (IL)-6, IL-10, matrix metalloproteinase-9, and interferon-γ. Transfusion caused or exacerbated changes in monocyte chemotactic protein-1, IL-1α, IL-5, IL-15, and soluble E-selectin. Finally, trauma and hemorrhage alone increased CXCL1 and IL-13.

CONCLUSIONS: This work provides a detailed characterization of the major shift in the immunologic environment in response to trauma and transfusion and clarifies which immune mediators are affected by trauma and hemorrhage and which by transfusion.

Ancillary