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Mediators of Inflammation
Volume 2015 (2015), Article ID 691491, 9 pages
Research Article

Role of the RAGE Axis during the Immune Response after Severe Trauma: A Prospective Pilot Study

1Department of Anesthesiology, Heidelberg University Hospital, 69120 Heidelberg, Germany
2Department of Medicine I and Clinical Chemistry, Heidelberg University Hospital, 69120 Heidelberg, Germany
3Department of Anaesthesiology and Intensive Care Medicine, Justus-Liebig-University, 35392 Giessen, Germany
4Department of General and Thoracic Surgery, Justus-Liebig-University, 35392 Giessen, Germany
5Department of Trauma, Hand and Reconstructive Surgery, University Hospital of Giessen-Marburg GmbH, Campus Giessen, 35392 Giessen, Germany

Received 6 October 2015; Revised 24 November 2015; Accepted 9 December 2015

Academic Editor: Marc Pouliot

Copyright © 2015 Florian Uhle 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.


Background. Severe traumatization induces a complex pathophysiology, driven by the patient’s own immune system. The initial activation is a result of damage-associated molecular patterns, which are released from disrupted and dying cells and recognized by immune receptors, for example, RAGE. In this study we aimed to evaluate the contribution of the RAGE axis to early and late immune responses. Methods. We enrolled 16 patients with severe trauma together with 10 patients after major abdominal surgery and 10 healthy volunteers. Blood samples were taken on admission and every 48 h for a total of 8 days. Plasma concentrations of various RAGE ligands as well as RAGE isoforms and IL-6 were measured by ELISA. Monocyte surface expression of RAGE and HLA-DR was assessed by flow cytometry. Results. High and transient levels of IL-6 and methylglyoxal characterize the early immune response after trauma, whereas samples from later time points provide evidence for a secondary release of RAGE ligands. Conclusion. Our results provide evidence for a persisting activation of the RAGE axis while classical mediators like IL-6 disappear early. Considering the immunocompromised phenotype of the monocytes, the RAGE ligands might be substantial contributors to the well-known secondary stage of impaired immune responsiveness in trauma patients.