%0 Journal Article
%T Immunoinflammatory Response in Critically Ill Patients: Severe Sepsis and/or Trauma
%A Maja Surbatovic
%A Milic Veljovic
%A Jasna Jevdjic
%A Nada Popovic
%A Dragan Djordjevic
%A Sonja Radakovic
%J Mediators of Inflammation
%D 2013
%I Hindawi Publishing Corporation
%R 10.1155/2013/362793
%X 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. 1. Some of the New Elements of Immunoinflammatory Response in Severe Sepsis Infection has been the leading cause of death in humans, since the earliest written sources. In the early 15th century, the black death plague wiped out between one-third and one-half of the entire European and Asian populations. The Greek word ¡°sepo,¡± from which the term ¡°sepsis¡± derives, means ¡°decomposition of animal, or vegetable or organic matter in the presence of bacteria¡± [1]. Modern cytokine research began in 1932, with the pioneer work of Rich and Lewis, who first observed antigen-mediated inhibition of leukocyte migration in tuberculin-sensitized tissue. Cytokine biology expanded 30 years ago, and the term ¡°cytokine¡± was first used by Cohen, referring to the variety of soluble factors, with wide range of biological activities related to immune system, produced by wide range of cell types [2]. In 1975, Carswell described the pivotal role of tumor necrosis factor, as one of the earliest monokines, in severe sepsis [3]. At first, this cytokine was also called ¡°cahectin,¡± which describes its ability to suppress lipoprotein lipase activity, leading to hypertriglyceridemia and rapid weight loss in experimental animals [4]. Interactions between infecting microorganisms and host response can lead to severe sepsis and septic shock. In response to pathogen adherence to an epithelial surface, the host initiates specific mucosal defense mechanisms, in order to prevent microbial invasion. The critical bacterial density needed to initiate an infection is called quorum. Bacterial cell-to-cell communication enables them to assess their population density and interact with the host as a population (quorum-sensing systems). Innate immunity¡ªrepresenting early non-specific response system¡ªand adaptive immunity¡ªrepresenting more pathogen-specific response system¡ªare parts of immune system as a whole [5]. The inflammatory response of the host is similar, regardless of the nature of the stimuli (infectious or noninfectious, like tissue injury). Initially, microorganisms bind to surface Toll-like receptors (TLRs) on phagocytic cells. These receptors are
%U http://www.hindawi.com/journals/mi/2013/362793/