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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
Stress, a state of threatened homeostasis, may be induced by various physical or psychological factors (stressors), including antigenic stimulation. Stressful experiences may affect both physical/psychological well being and immune functioning of humans and animals; the ongoing immune reaction may affect other physiological functions and psychological comfort. The molecular basis of these effects involves a network of multidirectional signalling and feedback regulations of neuroendocrine- and immunocyte-derived mediators. The consecutive stages of the multistep immune reactions might be either inhibited or enhanced owing to the previous and/or parallel stress experiences, depending on the kind of stressor and the animal species, strain, gender, or age. Therefore, the final results of stress-induced alteration of immune reactions are difficult to predict. The effect of a particular stressor on immune functions varies according to the previous stress experience of the individual (e.g. social confrontation, sterile saline injection) while various stressors may act in the same or in opposite ways on the same immune parameter. In general, the efficacy of immune response depends on the neuroendocrine environment on which it is superimposed. Conversely, neural and endocrine responses depend on the concurrent immune events upon which they are superimposed. It seems that the consequences of stress on the immune functioning are generally adaptive in the short run but can be damaging when stress is chronic.
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