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Analysis of Immune Mediator Production Following Traumatic Brain Injury

  • T. Kossmann
  • V. H. J. Hans
  • P. M. Lenzlinger
  • E. Csuka
  • P. F. Stahel
  • O. Trentz
  • M. C. Morganti-Kossmann
Conference paper

Abstract

Patients with severe head injury still carry a high risk of mortality and morbidity despite progress in clinical management (Frankowski et al. 1985; Alberico et al. 1987). Major causes of mortality in these patients are untreatable elevated intracranial pressure (ICP) in the early phase and septic-infectious complications during the later phase (Shackford et al. 1989). The importance of inflammatory events following head trauma even in the absence of systemic injuries has been recognized. Within a short period of time after hospitalization these patients show a depressed T-cell function, an anergy to delayed-type hypersensitivity skin testing, a decrease in the expression of interleukin-2 receptors on T-cells and, furthermore, a diminished in vitro interleukin-2 and γ-interferon production of T-cells as well as suppressed cell cytotoxicity (Quattrocchi et al. 1991; Hoyt et al. 1990). However, the depression of the peripheral immune system may be of a secondary nature and may be regulated by immunological events initiated as a result of the traumatic injury within the brain. In particular cytokines produced and released in the central nervous system (CNS) may play important roles in the pathophysiological events following brain trauma.

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Copyright information

© Springer-Verlag Berlin Heidelberg 1997

Authors and Affiliations

  • T. Kossmann
  • V. H. J. Hans
  • P. M. Lenzlinger
  • E. Csuka
  • P. F. Stahel
  • O. Trentz
  • M. C. Morganti-Kossmann

There are no affiliations available

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