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EN
The concept of four cardinal signs of acute inflammation comes from antiquity as rubor et tumor cum calore et dolore, extended later by functio laesa (redness and swelling with heat and pain, extended later by loss of function). The contemporary understanding of this process we owe to nineteen-century milestone discoveries by Rudof Virchow, Julius Cohnheim, and Elie Metchnikoff. In twentieth century, the development of potent technological tools allowed the rapid expansion of knowledge of cells and mediators of inflammatory processes, and molecular mechanisms of their interactions. It turned out that some mediators of inflammation have both local and distant targets, among them the liver (responding by production of several acute phase reactants) and neurohormonal centres. In the last decades it has become clear that the immune system shares mediators and their receptors with the neurohormonal system of the body; thus they form a common homeostatic entity. Such an integrative view, introduced by J.Edwin Blalock, when combined with Hans Selye?s concept of stress, led to the contemporary understanding of sickness behaviour, defined by Robert Dantzer as a highly organised strategy of the organism to fight infections and to respond to other environmental stressors.
EN
Mechanical trauma is one of the most important causes of morbidity in the developed world. The response of the immune system to mechanical insult is of paramount importance for the patient's recovery. Shortly after trauma, the indiscriminate saystemic inflammatory response syndrome (SIRS) is mediated by circulating monocytes (Ms) and other innate immunity components. Then acquired immunity, limited to the offending pathogen and the site of injury, gradually preponderates. SIRS is followed by the compensatory anti-inflammatory response syndrome (CARS), where the initial inflammatory response is quenched by anti-inflammatory mediators. This precisely regulated process of immune system activation in response to trauma can be easily deviated, resulting in multi-organ failure (MOF) and increased mortality. Excessive activation of inflammatory Ms in the SIRS phase, premature or exorbitant CARS, a predominance of macrophages (Macs) in the blood stream and peripheral tissues, as well as a depletion of dendritic cells are often seen in trauma patients and contribute to the development of MOF. Here we explore several mechanisms of pathological M? activation in patients with severe mechanical traumatic injury without accompanying sepsis.
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