Abstract
Immunoinflammatory response in critically ill patients is very complex. This review explores some of the new elements of immunoinflammatory response in severe sepsis, tumor necrosis factor-alpha in severe acute pancreatitis as a clinical example of immune response in sepsis, immune response in severe trauma with or without secondary sepsis, and genetic aspects of host immuno-inflammatory response to various insults in critically ill patients.
Highlights
Immunoinflammatory response in critically ill patients is very complex
This review explores some of the new elements of immunoinflammatory response in severe sepsis, tumor necrosis factor-alpha in severe acute pancreatitis as a clinical example of immune response in sepsis, immune response in severe trauma with or without secondary sepsis, and genetic aspects of host immunoinflammatory response to various insults in critically ill patients
Besides pathogen associated molecular patterns (PAMPs), there are several endogenous molecules, such as high-mobility group box(HMGB-) 1, hyaluronan, and heat-shock proteins (HSPs) that are able to trigger the immune response through pattern recognition receptors (PRRs)
Summary
Immunoinflammatory response in critically ill patients is very complex. This review explores some of the new elements of immunoinflammatory response in severe sepsis, tumor necrosis factor-alpha in severe acute pancreatitis as a clinical example of immune response in sepsis, immune response in severe trauma with or without secondary sepsis, and genetic aspects of host immunoinflammatory response to various insults in critically ill patients. The explanation of SIRS in absence of obvious microbial infection was provided by Matzinger [10], elucidating host response to DAMPs that can activate innate immunity through, among others, TLRs. Severe sepsis and/or trauma complicated with multiple organ dysfunction syndrome (MODS) are leading causes of death in intensive therapy units with mortality rate exceeding 50%.
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