Posttraumatic Immune Response and Its Modulation

Copyright © 2012 Frank Hildebrand 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. Following accidental trauma, an inflammatory response is induced involving hormonal, metabolic, and immunological mediators. This posttraumatic immune response is a physiological process required for tissue repair and regulation of the healing process. An overwhelming response after major trauma causes a disbalance between pro-and anti-in-flammatory mediators resulting in complications like an increased susceptibility to infection, sepsis, and the Multior-gan-Dysfunction-Syndrome (MODS) [1]. Therefore, profound knowledge of this inflammatory response is a major interest in order to anticipate and control these potential posttraumatic complications. Following major trauma, a local release of mediators such as cytokines, acid metabolites, and histamine increases the capillary permeability resulting in tissue edema and local infiltration of immunocompetent cells. Intrinsic leukocytes and affected endothelial cells produce and release pro-and anti-inflammatory cytokines acting locally as well as on remote cells in different organs like the lung [1, 2]. In this issue P. Mommsen et al. investigated the role of IL-6 on cytokine production capacity of splenocytes after femoral shaft fracture, isolated or in combination with hemorrhage in male mice. The authors showed that an isolated femoral fracture resulted in a suppression of in vitro cytokine synthesis of splenocytes, which was further enhanced in case of an additional hemorrhagic shock. In IL-6 knockout mice, the splenic immunodepression after femoral fracture and hemorrhagic shock attenuated. These results give evidence that the posttraumatic modulation of IL-6 synthesis might be a potential target for therapeutic interventions. As contradictory findings in animal models of trauma and sepsis impede a rationale for therapies directed against IL-6 in general , selective inhibition of IL-6 transsignaling using soluble IL-6R seems to be a potential treatment strategy [3]. P. Kobbe et al. (in this issue) described the effects of inha-lative IL-10 administration on the pulmonary and systemic inflammatory response after hemorrhage in male mice. The authors found that inhalative IL-10 application resulted in a significant decrease of the inflammatory reaction in the lung without affecting the systemic immune response after hemorrhage. From the clinical point of view, generally the lung is the first organ to fail after injury. Furthermore, respiratory failure is most frequent in patients developing MODS, and these patients have the highest mortality rate [4]. Therefore, the results of P. …