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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.
EN
Recently, the role of small heat shock proteins (HSPs) has been widely recognized in cancer research. Small HSPs are tumor-protective via numerous, independent mechanisms such as: oxidative stress protection preventing protein denaturation, anti-apoptotic activity, and likely direct suppression of the immune system. However, it is unclear whether they play any role in the initial steps in carcinogenesis. This article seeks to familiarize the reader with general characteristics of small HSPs (especially HSP-27, A/B-crystallins), tissue distribution with special regard on their expression in malignant specimens, and biological properties of intracellular HSP-27 and A/B-crystallins promoting tumor genesis and growth. A separate chapter describes immunomodulatory characteristics of extracellular HSP-27 with special emphasis on their plausible effect on the neoplasm development.
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