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EN
Overtraining is a maladaptive state of athlete’s body related to the physical, behavioral and emotional condition, occurring when exercise training exceeds the recoverability. The cytokine hypothesis of overtraining promoted in recent years is seen as the prevailing theory explaining the understanding of the overtraining phenomenon. The high level of pro-inflammatory cytokines (IL-6, TNFα, IL-1β) involved in the inflammatory response may strongly influence not only the central nervous system but also the endocrine and immune systems. Moreover, there is a range of factors in athlete’s life that appear to increase the risk of depression development, such as psychological and emotional stress associated with sports competition. The aim of this review was to reveal the role of high level of proinflammatory cytokines observed in OTS with the possible occurrence of depression symptoms in athletes. Latest findings have shown an important role of the same pro-inflammatory cytokines in the development of depression. The study discusses a potential mechanism responsible for the development of depression in athletes, which may be helpful in the quick diagnosis of depression basis in athletes. Due to the low number of studies concerning depression and inflammation in athletes further research should be conducted.
EN
Kinins, universal mediators of inflammation, are recognized by two kinds of receptors, B1 and B2, which have been found to be expressed in numerous cell types of several species. However, the knowledge of the regulation of these receptors in leukocytes is still not satisfactory. In the current work, we have demonstrated a constitutive production of B2 receptor mRNA in the human promonocyte U937 cells and its two-fold augmentation after cell differentiation with retinoic acid and phorbol ester. Bradykinin and des-Arg10-kallidin induced the expression of both B2 and B1 receptors in cells before and after differentiation. Generally, the undifferentiated cells were more susceptible to bradykinin-dependent induction of kinin receptors (increases by approximately 250% and 200% for B2 and B1 receptors, respectively). The induction, by approx. 200%, of B1 receptor by des-Arg10-kallidin was detected on both mRNA and protein levels. In addition, an unexpected strong induction of B2 receptor by this compound was observed in the retinoic acid- and phorbol ester-differentiated cells (by 150% and 200%, respectively) that suggests a possible autoregulation of kinin receptors by own agonists during the inflammatory state. On the other hand, a strong enhancement of the expression of both receptors by interleukin 1β, especially in the phorbol ester-differentiated cells, indicates the involvement of kinin receptors in the propagation of the inflammatory processes.
PL
Proces zapalny jest bezpośrednio związany z sekrecją cytokin, np. czynnika martwicy nowotworu alfa (ang. Tumor Necrosis Factor alpha; TNF-α). Ta cząsteczka jest 1 z 22 białek należących do rodziny TNF i wydzielana jest głównie przez: makrofagi, monocyty, limfocyty T oraz komórki tuczne. Biologiczne efekty działania TNF-α zachodzą dzięki wiązaniu się tej cytokiny ze specyficznymi dla niej receptorami – TNFR1 i TNFR2. Duża liczba prac potwierdza kluczową rolę TNF-α w nowotworzeniu i chorobach układu sercowo-naczyniowego, będących chorobami o podłożu prozapalnym. Niestety, mimo postępu medycyny i wzrostu świadomości społeczeństwa, wymienione choroby stanowią główne przyczyny śmierci na świecie. Lepsze zrozumienie roli tej cytokiny w kancerogenezie i chorobach zapalnych może spowodować wykorzystanie TNF-α jako markera tych chorób oraz do monitorowania przeciwzapalnych efektów terapii.
EN
The inflammatory process is directly associated with secretion of cytokines, e.g. tumor necrosis factor alpha (TNF-α). This molecule is one of the 22 proteins which belong to TNF family and is secreted mainly by: macrophages, monocytes, T lymphocyte and mast cells. The biological effects of TNF-α is possible through binding this cytokine to specific receptors – TNFR1 and TNFR2. The large number of reports provides that this cytokine plays extremely important role in cancers and cardiovascular disease – two groups of inflammatory diseases. Unfortunately, these diseases are the main cause of death in spite of advances in medicine and increasing public awareness of prevention. It is believed that better understanding both molecular potential of this cytokine and the impact in cancerogenesis and others inflammatory diseases may cause using TNF-α as a molecular marker in these diseases and will make it possible to observe the effects of anti-inflammatory therapy. It will be able to cause a drop in the incidence of these diseases and better monitoring of them.
17
Content available remote Interleukin-6 biology is coordinated by membrane bound and soluble receptors.
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EN
Cytokine receptors exist in membrane bound and soluble form. Both forms bind their ligands with comparable affinity. While most soluble receptors are antagonists in that they compete for the ligands with their membrane counterparts, some soluble receptors are agonists. In this case, the complex of ligand and soluble receptor binds on target cells to a second receptor subunit and initiates signal transduction. Soluble receptors of the IL-6 family of cytokines are agonists. In vivo, the IL-6/soluble IL-6R complex stimulates several types of target cells not stimulated by IL-6 alone, since they do not express the membrane bound IL-6R. This process has been named transsignaling. We have shown that in several chronic inflammatory diseases like chronic inflammatory bowl disease, peritonitis and rheumatoid arthritis, transsignaling via the soluble IL-6R complexed to IL-6 is a crucial point in the transition from the acute to the chronic state of the disease. The mechanism by which the IL-6/ soluble IL-6R complex regulates the inflammatory state is discussed.
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