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Introduction The gastrointestinal tract is a barrier from harmful substances, this protection is provided by the association of epithelial and immune cells, alongside resident gut microbiota [ 1 ]. Gut microbiota plays important role in host

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scanty reports on the influence of high dietary salt consumption on the immune system. Okuda and Grollman ( 14 ) reported that hypertension can be induced in normotensive rats by transferring lymphocytes from hypertensive rats. This suggested that

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Hormonal imprinting is an epigenetic process which is taking place perinatally at the first encounter between the developing hormone receptors and their target hormones. The hormonal imprinting influences the binding capacity of receptors, the hormone synthesis of the cells, and other hormonally regulated functions, as sexual behavior, aggressivity, empathy, etc. However, during the critical period, when the window for imprinting is open, molecules similar to the physiological imprinters as synthetic hormone analogs, other members of the hormone families, environmental pollutants, etc. can cause faulty imprinting with life-long consequences. The developing immune system, the cells of which also have receptors for hormones, is very sensitive to faulty imprinting, which causes alterations in the antibody and cytokine production, in the ratio of immune cells, in the defense against bacterial and viral infections as well as against malginant tumors. Immune cells (lymphocytes, monocytes, granulocytes and mast cells) are also producing hormones which are secreted into the blood circulation as well as are transported locally (packed transport). This process is also disturbed by faulty imprinting. As immune cells are differentiating during the whole life, faulty imprinting could develop any time, however, the most decisive is the perinatal imprinting. The faulty imprinting is inherited to the progenies in general and especially in the case of immune system. In our modern world the number and amount of arteficial imprinters (e.g. endocrine disruptors and drugs) are enormously increasing. The effects of the faulty imprinters most dangerous to the immune system are shown in the paper. The present and future consequences of the flood of faulty imprintings are unpredictable however, it is discussed.

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Stress caused by 48 h food and water deprivation provoked significant changes in T3 and serotonin content of lymphocytes. The concentration of these hormones decreased in the last hour of stress. However, 48 h later there was no difference between the hormone content of immune cells of stressed and control animals. Since in earlier experiments three weeks after exposed to stress a significant difference between the control and stressed animals was found, this means that an imprinting-like phenomenon happened with consequences manifested later. The most sensitive cells to acute stress are lymphocytes, however the imprinting influences all types of of the immune cells.

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According to experimental data, eukaryote unicellulars are able to learn, have immunity and memory. Learning is carried out in a very primitive form, and the memory is not neural but an epigenetic one. However, this epigenetic memory, which is well justified by the presence and manifestation of hormonal imprinting, is strong and permanent in the life of cell and also in its progenies. This memory is epigenetically executed by the alteration and fixation of methylation pattern of genes without changes in base sequences. The immunity of unicellulars is based on self/non-self discrimination, which leads to the destruction of non-self invaders and utilization of them as nourishment (by phagocytosis). The tools of learning, memory, and immunity of unicellulars are uniformly found in plasma membrane receptors, which formed under the effect of dynamic receptor pattern generation, suggested by Koch et al., and this is the basis of hormonal imprinting, by which the encounter between a chemical substance and the cell is specifically memorized. The receptors and imprinting are also used in the later steps of evolution up to mammals (including man) in each mentioned functions. This means that learning, memory, and immunity can be deduced to a unicellular eukaryote level.

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Lectures on phagocytosis and immunity Br Med J 1 213 217 . 2. RA Nelson Jr

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) Flaherty , Edward , ‘ The Abuse of Functional Immunity Party Almost Over Last chance, last call? ’ ( 2003 ) 620, UN Special 2003 Archives. Gaillard , Emmanuel and Pingel

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Acta Microbiologica et Immunologica Hungarica
Authors:
Farhad Riazi-Rad
,
Ava Behrouzi
,
Hoora Mazaheri
,
Asal Katebi
, and
Soheila Ajdary

systemic functions, including metabolism, energy balance [ 2 ], immunity, and inflammation [ 3 ]. Host genetics, such as genetic variations in immunity-related pathways, can impact the microbiota's composition at various anatomical sites [ 4 ]. The host

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Orvosi Hetilap
Authors:
János László Iványi
,
Éva Marton
, and
Márk Plander

Borbényi, Z.: Diagnostic and therapeutic options in adults with primary immune thrombocytopenia: recommendation of the National Advisory Board. [Diagnosztikus és kezelési ajánlás felnőttkori primer

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living world from deleterious effects as it is done by the immune system, but preceding this latter and also collaborating with it. It is estimated that centuries ago, the natural background radiation was about fivefold larger than in recent times and

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