• S Weiterer, F Uhle, B H Siegler, C Lichtenstern, M Bartkuhn, and M A Weigand.
• Klinik für Anästhesiologie, Universitätsklinikum Heidelberg, Im Neuenheimer Feld 110, 69120, Heidelberg, Deutschland, Sebastian.Weiterer@med.uni-heidelberg.de.
• Anaesthesist. 2015 Jan 1;64(1):42-55.

AbstractSepsis is known to be a severe systemic immune reaction based on an infection of various origins. The initial immune response is accompanied by excess activation of immune cells and release of proinflammatory cytokines. Simultaneously initiated compensatory mechanisms lead to high levels of anti-inflammatory mediators to counterbalance the generalized inflammatory reaction; however, the compensatory immunoreaction itself equally overreacts and results in a prolonged sepsis-induced immunosuppression. The underlying mechanisms for these exaggerated immune responses and the resulting global immunosuppression that increase the risk for secondary infection are still unknown. Recent findings indicate that epigenetic mechanisms change basic properties of important immune cells by mechanisms leading to changes in gene expression. Dynamic exchanges of histone modifications result in a variation of transcription and seem to play a key role in cell function of macrophages and other immune cells. This article provides a current overview of epigenetic sepsis research and the sepsis-induced effects on the immune system.

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