Immune Reactions after Trauma

Abstract

Activation of the immune system for wound healing following accidental trauma is a well-studied phenomenon. The reaction comprises both the cellular and humoral systems. The various steps in the reaction are all temporally defined and influence each other. The main cells involved are polymorphonuclear granulocytes (PMN), monocytes, and lymphocytes. They interact and adhere to the endothelium via adhesion molecules such as L-selectin and ICAM-1. The humoral mediators discussed in this review are tumor necrosis factor-␣ (TNF-␣) and its receptors, interleukin-1␤ (IL-1␤), IL-6, IL-10 and interferon-␥ (IFN-␥). The kinetics of the cells appearing and of the cytokines are discussed. The actions of these players are reviewed along with the most recent literature. Furthermore, we attempt to elucidate causal relationships. The immune system can be hyper-or hypoactive. Both exaggerated pro-and antiinflammatory reactions may have the same endpoint: multiple organ dysfunction syndrome (MODS). This knowledge should be used to meticulously monitor the patient's immunologic status. Depending on the state, hyper-or hypoinflammatory, the treatment should comprise anti-inflammatory and immune-restoring properties, respectively. What is decisive to survival is timely, adequate management based on the individual patient's status.

Temporal Profile of Cerebrospinal Fluid, Plasma, and Brain Interleukin-6 After Normothermic Fluid-Percussion Brain Injury: Effect of Secondary Hypoxia

“…After stroke, for example, elevated levels of IL-6 are associated with the infarct size and poor outcome (Vila et al, 2000;Smith et al, 2004;Waje-Andreassen et al, 2005). In this regard, IL-6 levels are considered a highly specific biomarker of TBI severity and long-term outcome (van Griensven et al, 2003;Howell et al, 2006). In addition, IL-6 plays an important role in activating and recruiting immune cells and has been reported to suppress TNF-a and IL-1-b production and stimulate nerve growth factor (NGF) production (Kushima et al, 1992;Juttler al., 2002).…”

Immune Modulation after Total Hip Surgery

“…The mechanism of this 'endotoxin tolerance' is not clearly understood [38] , but TNF-␣ production or release may be downregulated by anti-inflammatory cytokines as well as by several factors that initiate intracellular formation of cAMP [39][40][41][42] . An overwhelming anti-inflammatory response (hypoinflammation) seems to be responsible for posttraumatic immunosuppression with susceptibility to infections and septic complications [14,27,43] .…”

“…Following the proinflammatory reaction, anti-inflammatory mediators are produced to avoid autodestructive effects of immune competent cells [13,14,27] . Several cytokines have shown a dual effect with pro-and antiinflammatory activities.…”

“…The inflammatory responses are characterized by local and systemic production and release of different mediators, such as proinflammatory cytokine [11][12][13][14] . The systemic release of proinflammatory cytokines, especially IL-6, induces the acute phase reaction in the liver with synthesis of acute phase proteins to enhance tissue-protective and antimicrobial mechanisms.…”

Effects of changing strategies of fracture fixation on immunologic changes and systemic complications after multiple trauma: Damage control orthopedic surgery

“…When we altered our management of patients by reducing the duration of initial surgery, we observed that this lead to a reduction in unexpected complications (e.g., ARDS) following the initial surgery, but were unable to explain this effect until immunologic monitoring became available. 20,28,37,39,41,44,[76][77][78][79][80][81][82][83][84][85][86][87] The models of biological response to different stimuli (trauma and major surgeries) have then become the basis of treatment. The principle of limiting surgery is therefore founded on the concept of minimizing the degree of the second hit impact, that is, the inflammatory stimulus.…”