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Journal of Transplantation
Volume 2013, Article ID 521369, 19 pages
http://dx.doi.org/10.1155/2013/521369
Review Article

Inflammatory Signalling Associated with Brain Dead Organ Donation: From Brain Injury to Brain Stem Death and Posttransplant Ischaemia Reperfusion Injury

1Critical Care Research Group, The Prince Charles Hospital, Rode Road, Chermside, QLD, Australia
2Department of Emergency Medicine, Princess Alexandra Hospital, 199 Ipswich Road, Woolloongabba, QLD, Australia

Received 8 June 2012; Revised 19 January 2013; Accepted 22 January 2013

Academic Editor: Gaetano Ciancio

Copyright © 2013 Ryan P. Watts et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Brain death is associated with dramatic and serious pathophysiologic changes that adversely affect both the quantity and quality of organs available for transplant. To fully optimise the donor pool necessitates a more complete understanding of the underlying pathophysiology of organ dysfunction associated with transplantation. These injurious processes are initially triggered by catastrophic brain injury and are further enhanced during both brain death and graft transplantation. The activated inflammatory systems then contribute to graft dysfunction in the recipient. Inflammatory mediators drive this process in concert with the innate and adaptive immune systems. Activation of deleterious immunological pathways in organ grafts occurs, priming them for further inflammation after engraftment. Finally, posttransplantation ischaemia reperfusion injury leads to further generation of inflammatory mediators and consequent activation of the recipient’s immune system. Ongoing research has identified key mediators that contribute to the inflammatory milieu inherent in brain dead organ donation. This has seen the development of novel therapies that directly target the inflammatory cascade.