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Role of Complement on Broken Surfaces After Trauma

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Immune Responses to Biosurfaces

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 865))

Abstract

Activation of both the complement and coagulation cascade after trauma and subsequent local and systemic inflammatory response represent a major scientific and clinical problem. After severe tissue injury and bone fracture, exposure of innate immunity to damaged cells and molecular debris is considered a main trigger of the posttraumatic danger response. However, the effects of cellular fragments (e.g., histones) on complement activation remain enigmatic. Furthermore, direct effects of “broken” bone and cartilage surfaces on the fluid phase response of complement and its interaction with key cells of connective tissues are still unknown. Here, we summarize data suggesting direct and indirect complement activation by extracellular and cellular danger associated molecular patterns. In addition, key complement components and the corresponding receptors (such as C3aR, C5aR) have been detected on “exposed surfaces” of the damaged regions. On a cellular level, multiple effects of complement activation products on osteoblasts, osteoclasts, chondrocytes and mesenchymal stem cells have been found.

In conclusion, the complement system may be activated by trauma-altered surfaces and is crucially involved in connective tissue healing and posttraumatic systemic inflammatory response.

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Acknowledgments

The cited author’s own work was funded in part by the State of Baden-Württemberg (Perspektivförderung), the DFG Clinical Research Unit KFO200 TP2 and TP4, and the SFB1149.

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Correspondence to Markus Huber-Lang .

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Huber-Lang, M., Ignatius, A., Brenner, R.E. (2015). Role of Complement on Broken Surfaces After Trauma. In: Lambris, J., Ekdahl, K., Ricklin, D., Nilsson, B. (eds) Immune Responses to Biosurfaces. Advances in Experimental Medicine and Biology, vol 865. Springer, Cham. https://doi.org/10.1007/978-3-319-18603-0_3

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