2013
DOI: 10.1155/2013/362793
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Immunoinflammatory Response in Critically Ill Patients: Severe Sepsis and/or Trauma

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.

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Cited by 55 publications
(51 citation statements)
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“…7 The poorly regulated inflammatory ''storm'' of sepsis has been reviewed extensively elsewhere. 8,9 Despite decades of basic science and clinical research, it remains unclear how absolute or relative concentrations, or timing of interactions of inflammatory mediators effects the evolution of inflammation and ultimately how manipulation of these mediators may become therapeutic options. Furthermore, complex interactions between inflammation, endogenous anti-inflammatory processes, coagulation and platelets, and the and most workers feel our understanding of manipulating inflammation has moved beyond the ''magic bullet'' single intervention.…”
Section: Discussionmentioning
confidence: 99%
“…7 The poorly regulated inflammatory ''storm'' of sepsis has been reviewed extensively elsewhere. 8,9 Despite decades of basic science and clinical research, it remains unclear how absolute or relative concentrations, or timing of interactions of inflammatory mediators effects the evolution of inflammation and ultimately how manipulation of these mediators may become therapeutic options. Furthermore, complex interactions between inflammation, endogenous anti-inflammatory processes, coagulation and platelets, and the and most workers feel our understanding of manipulating inflammation has moved beyond the ''magic bullet'' single intervention.…”
Section: Discussionmentioning
confidence: 99%
“…The presence of pathogens in blood or in tissues leads to the activation of systemic inflammatory process, which results in a nonspecific response from the organism (Surbatovic et al 2013). Through this synergic or antagonist action of pro-inflammatory mediators, a series of molecular modifications are produced, which later on affects the structure and function of the cell.…”
Section: Pathophysiology Of Sepsismentioning
confidence: 99%
“…Severe trauma, irrespective of mechanism, commonly causes substantial amounts of blood loss leading to decreased endothelial derived Nitric Oxide (NO), which further leads to augmented platelet aggregation, increased neutrophil infiltration and deregulation of vasorelaxation (Surbatovic et al, 2013). As expected with trauma, loss of endothelial integrity increases vascular permeability, characteristic of the innate immune response reacting to DAMPs.…”
Section: Deterioration Of the Immune System After Traumamentioning
confidence: 99%