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Mediators of Inflammation
Volume 2012 (2012), Article ID 136020, 7 pages
Research Article

Systemic Inflammatory Effects of Traumatic Brain Injury, Femur Fracture, and Shock: An Experimental Murine Polytrauma Model

1Department of Trauma and Orthopaedic Surgery, Cologne Merheim Medical Center, Faculty of Health-School of Medicine, Witten/Herdecke University, Ostmerheimer Straße 200, 51109 Cologne, Germany
2Department of Trauma, Neurosurgery, Hannover Medical School, 30623 Hannover, Germany
3Department of Traumatology, Hannover Medical School, 30623 Hannover, Germany
4Department of Anaesthesiology, Nordstadt Hospital Hannover, 30167 Hannover, Germany
5International Neuroscience Institute Hannover, Department of Neurosurgery, 30625 Hannover, Germany
6Institute of Experimental Traumatology, University of Technology-Munich, 81675 München, Germany

Received 13 October 2011; Accepted 6 December 2011

Academic Editor: Frank Hildebrand

Copyright © 2012 C. Probst 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.


Objective. Despite broad research in neurotrauma and shock, little is known on systemic inflammatory effects of the clinically most relevant combined polytrauma. Experimental investigation in an animal model may provide relevant insight for therapeutic strategies. We describe the effects of a combined injury with respect to lymphocyte population and cytokine activation. Methods. 45 male C57BL/6J mice (mean weight 27 g) were anesthetized with ketamine/xylazine. Animals were subjected to a weight drop closed traumatic brain injury (WD-TBI), a femoral fracture and hemorrhagic shock (FX-SH). Animals were subdivided into WD-TBI, FX-SH and combined trauma (CO-TX) groups. Subjects were sacrificed at 96 h. Blood was analysed for cytokines and by flow cytometry for lymphocyte populations. Results. Mortality was 8%, 13% and 47% for FX-SH, WD-TBI and CO-TX groups ( ). TNFα (11/13/139 for FX-SH/WD-TBI/CO-TX; ), CCL2 (78/96/227; ) and IL-6 (16/48/281; ) showed significant increases in the CO-TX group. Lymphocyte populations results for FX-SH, WD-TBI and CO-TX were: CD-4 (31/21/22; n.s.), CD-8 (7/28/34, ), CD-4-CD-8 (11/12/18; n.s.), CD-56 (36/7/8; ). Conclusion. This study shows that a combination of closed TBI and femur-fracture/ shock results in an increase of the humoral inflammation. More attention to combined injury models in inflammation research is indicated.