The acute inflammatory response underlies the pathophysiological mechanisms involved in the development of MODS. The plasma cascades are also activated which together with the produced pro-inflammatory mediators stimulate further the production of inflammatory biomarkers. The sensed danger signals, through specific signalling pathways, activate nuclear transcription factor κB and other transcription factors and gene regulatory systems which up-regulate the expression of pro-inflammatory mediators. This response starts with sensing of danger by pattern-recognition receptors on the immune competent cells and endothelium. In critical illness, the acute immune response is organized and executed by innate immunity influenced by the neuroendocrine system. critical illness) remain high despite advances in diagnostic and organ supporting possibilities in intensive care units. The mortality and morbidity in SIRS and sepsis (i.e. The host inflammatory response in SIRS and sepsis is similar and may lead to multiple organ dysfunction syndrome (MODS) and ultimately death. The systemic immune response induced by non-infectious agents is called systemic inflammatory response syndrome (SIRS) and infection-induced systemic immune response is called sepsis.
