“The natural healing force within each one of us is the greatest force in getting well.” Hippocrates Prof. G.F. Solomon was one of the first scientists to hypothesize that the relationship between brain activity and the body’s immune system can be important for determining health and influencing the course of the disease and its outcome. John Solomon is the founder of psychoneuroimmunology, an interdisciplinary field of research into the interaction of the brain, behavior, and immune system that has played a key role in the study of behavioral and biological mechanisms that link psychosocial factors, health, and disease. His research helped to found a new area of knowledge - psychoneuroimmunology, which aims to uncover the mechanisms by which the brain is able to influence the functions of the immune system.

The levels proteins of control points of immunity sPD-1, sPD-L1 in serum or plasma of 366 patients with malignant tumors of various nosological forms treated at the N.N. Blokhin National Medical Research Center of Oncology. A correlation of sPD-L1 with the prevalence of the process and the degree of tumor malignancy, as well as a positive correlation with some other tumor markers of blood, was found: VEGF, VEGFR1, MMP-7, MMP-8, TIMP-1.

Introduction. There is increasing evidence that altered neuroimmune responses are implicated in the neurobiology of aggression, including the production of pro- and anti-inflammatory cytokines. However, little is known about brain cytokine changes and their regional characteristics in animals genetically selected for either high or low aggressive behaviors. Materials and methods. In the present study the content of cytokines (IL-1β, IL-2, IL-6, TNFα, IL-10) was measured by ELISA method in the brain structures (the hypothalamus, striatum, frontal cortex, and hippocampus) in two rat lines selected for differences in fear-induced aggression at 2, 4, and 24 h after a peripheral injection of saline or lipopolysaccharide (LPS, 250 µg/kg). Results and discussions. LPS stimulation elevated cytokine activity above baseline levels in both aggressive and nonaggressive rats, but the pattern, time course of cytokine changes, and their regional characteristics varied according to the aggressiveness of the animals. After LPS administration, aggressive rats showed increased levels of IL-1β in the hypothalamus at 2 and 4 h and in the frontal cortex at 4 and 24 h compared to LPS-treated nonaggressive line. IL-2 was increased in the frontal cortex and striatum of aggressive rats within 24 h, while IL-6 elevation in the hypothalamus was found at 4 h and in the frontal cortex at 2 and 4 h. In the hippocampus, the levels of IL-1β, IL-2, and IL-6 were lower in LPS-treated aggressive rats than in nonaggressive animals. The levels of anti-inflammatory cytokine IL-10 were also decreased in all brain structures of aggressive rats receiving LPS. Conclusion. The present data indicate that genetic predisposition to increased aggressiveness is associated with region-specific changes in the content of pro- and anti-inflammatory cytokines and their variations over time in the brain structures.

The aim of this work was to identify several markers of inflammation in the blood of patients with frontotemporal dementia (FTD). 34 patients were surveyed with FTD. The control group consisted of 35 age- and sex- matched healthy people. Blood plasma was used for immunological studies. The enzymatic activity of leukocyte elastase (LE) and the functional activity of the α1-proteinase inhibitor (α1-PI) were determined by a spectrophotometric method, the concentration of interleukin-6 (IL-6) and C-reactive protein (CRP) were measured by ELISE. A statistically significant increase in α1-PI activity (p < 0.0001) was detected in patients with FTD; no difference from control was found for other indicators. There is a significant variation in all indicators, i.e. both increase and decrease of values compared to the control group. According to the level of LE activity, two immunophenotypes were identified. 73.5% of patients with FTD have an immunophenotype characteristic of patients with endogenous psychosis and 26.5% of patients have an immunophenotype similar to Alzheimer’s disease. The data obtained indicate the involvement of inflammatory reactions in the development of FTD and the heterogeneity of this disease as assed by immunological parameters.

The aim. Detect the relationship between sympathetic activity, secretory alpha-amylase (sAA) indices and mediators of the immune system in healthy young volunteers (18-20 years) with correction drinking behavior (use pure water of 35 ml/(kg body weight)). Materials and methods. A randomized, placebo-controlled double-blind study, which was carried out in 3 stages (09/20/2014; 08/11/2014; 12/13/2014) into 3 groups (test, placebo and control). The material used was saliva, in which IL-1β, IL-4, IL-6 were detected by ELISA and the activity of alpha-amylase (sAA) was determined colorimetrically on an automatic analyzer; the level of sympathicotonia was determined by calculating the Kerdo-index. Results. A decrease in the activity of sAA test and placebo groups to the second stage, and the preservation of this trend in these groups by the end of the study, in contrast to the increase in its activity in the control group. The ratio of IL-1β/IL-6 at the third stage (MCC, p = 0.048) in the test and placebo groups (146.66 and 111.61, respectively) exceeded (by 3 times and 2.4 times respectively) this indicator control group. In a subpopulation with a predictor of inflammatory diseases (PID) of the oral cavity (IL-1β ≥ 212 pg/ml) of the experimental group, the average IL-1β decreased to the third stage by 27% (from 247.7 pg/ml to 194.4 pg/ml), in the placebo group, a similar decrease was 31.5% (from 243.24 pg/ml to 184.96 pg/ml), while in the control the level of IL-1β remained at the same level (about 250 pg/ml), p > 0.05. By the end of the research, the Kerdo index showed a predominance in the test group of participants with parasympathicotonia (66.67%), while in the placebo group this figure was 58.33%, and in the control 50%. Conclusion. The obtained data suggest an immunomodulatory effect of the use of 35 ml/(kg body weight) of pure water (clean by the physical method) against a decrease in sympathicotonia.

Pro-inflammatory cytokine IL-1β, as inflammatory mediators participate in neuroimmune interactions in the central nervous system. It’s assumed that IL-1β affect the central and peripheral breathing control in acute hypoxia that occurs simultaneously with systemic inflammation. The purpose of this study was to evaluate the influence IL-1β on respiratory responses following progressive hypoxia and ability to survive after hypoxic apnea. We studied the influence of IL-1β (10 μg/kg) on respiration and the ability to survive acute hypoxic challenge in anesthetized Wistar rats. The response of tidal volume, breathing rate, minute lung ventilation, oxygen saturation, during acute hypoxia was examined using pneumotachography methods. Increasing hypoxia was created by rebreathing method. The results indicated that during progressive acute hypoxia animals given IL-1β were unable to sustain breathing efforts for as long as control rats. Following hypoxic apnea IL-1β decrease the ability to autoresuscitate compared with control groups. Thus IL-1β reduces the tolerance of animals to acute hypoxia and the ability to spontaneously autoresuscitate after apnea. We assume that that IL-1β inhibit inspiratory neurons and decrease the sensitivity of the carotid chemoreceptors to hypoxic stimulation.

Introduction. It is known that the systemic level of the major pro-inflammatory cytokine increases in many respiratory diseases such as asthma, COPD and sleep apnea [1, 2]. The lung ventilation changes and the pathological types of breathing are typical in these diseases. By the reason, the research of the respiratory effects of cytokine is actual. The aim of this study was to compare the respiratory effects of tumor necrosis factor - α (TNF-α) before and after pretreatment with diclofenac, a nonspecific cyclooxygenase (COX) inhibitor. Materials and methods. Тhe experiments were performed in tracheostomized anaesthetized with urethane rats. A respiratory flow head connected to a pneumotachometer (AD Instruments ML141 Spirometer, Dunedin, New Zealand) was used to measure peak airflow and respiratory rate. The hypoxic ventilatory response was measured by using rebreathing with hypoxic gas mixture before and after the tail vein injection of TNF-α (10 μg/rat). In order to determine the role of the cyclooxygenase pathway in the ventilatory effects of TNF-α, introperitoneal administration of diclofenac, a nonspecific COX inhibitor, was used (0.5 mg/rat). Results and discussion. We have shown that the increase in level of TNF-α in blood increased the parameters of respiration such as minute ventilation (by 40%), tidal volume (by 18%), and the mean inspiratory flow (by 33%). The slope of the hypoxic ventilatory response decreased from 6.06 ± 0.91 to 3.48 ± 0.38 ml/min-1 mmHg-1 (by 40%) 40 min after administration of TNF-α (p < 0.05), the slope of tidal volume and mean inspiratory flow also decreased (by 27%) (p < 0.05). After pretreatment with diclofenac, the influence of TNF-α on breathing was dampened, as no significant changes were observed. Conclusion. We concluded that the elevation of inflammatory cytokine level in blood intensifies ventilation during the resting breathing that may be associated with increased central inspiratory activity. At the same time TNF-α reduces the chemoreflex sensitivity to hypoxia, thereby worsening the compensatory capabilities of the respiratory system. Thus, the results of our study suggest participation of inflammatory cytokines in mechanisms of central breathing control and chemoreception. Diclofenac pretreatment eliminated the respiratory effects of TNF-α. The data indicate that the ability of TNF-α to enhance basal ventilation and to reduce the ventilatory hypoxic response is mediated by the COX pathway.

The aim is to assess the levels of certain cytokines IL-6, TNF-α, IL-1β и IL-10, and BDNF in the blood plasma of the elderly, depending on degree of cognitive impairment. 65 elderly with (vascular dementia) or without cognitive impairment were enrolled in the study. The level of cytokines and BDNF were measured in plasma by ELISA. It was found that, regardless of the degree of cognitive impairment, the condition of systemic chronic low-grade inflammation is characteristic of the elderly. Against this background, plasma levels of BDNF were increased in elderly with vascular dementia, reaching statistical significance compared with healthy individuals. Such changes in the level of BDNF may reflect a compensatory repair mechanism in neurodegeneration or be associated with a defective axonal transport or utilization of BDNF in the central nervous system paralleled by increased serum concentrations.

Cytokine system and cartilaginous tissue metabolism of 27 women affected by 0-1 stage of primary and 19 women affected by 0-1 stage of post-traumatic osteoarthritis (OA) have been studied as well as of 10 healthy persons of the control group. The enzyme-linked immunoassay method was used to determine the content of cartilage oligometric matrix protein (СOMP), cartilage glucoprotein (YKL-40), interleukins (ILs) 4 and 1β in blood serum, collagen fragments (CTX II) in urine. It was found that СOMP, CTX II, YKL-40 and IL-1β concentrations grew at more intensive rate in case of primary OA compared to post-traumatic OA. The diminution of correlation relationship strength in IL-1β serum concentrations is noted with the system level of cartilaginous tissue degradation products on the background of YKL-40 regulatory influence buildup which is more prominent with primary OA than it is with the post-traumatic one. Conclusions: early stages of primary OA are characterized by more prominent degenerative changes in the joint hyaline cartilage due to losses of type II collagen and hyperproduction of proinflammatory link cytokines with the background of YKL-40 regulatory influence buildup and reduction of the IL-1β influence. The changes of cartilaginous tissue metabolism with post-traumatic OA were characterized by preservation of dependence on IL-1β serum concentration with the background of reduction of YKL-40 influence.

In the current study, biochemical abnormalities occurring in the body of children with cancer in sepsis, as well as their relationship with the new marker of sepsis and phagocytosis by presepsin, are considered. A survey enrolled 112 children who were treated at the N.N. Blokhin National Medical Research Center of Oncology. Differences in medians of a number of biochemical parameters in groups of patients who survived and died of sepsis were revealed.

Objective. We studied mast cells and neuroendocrine cells of the skin of adults in the area of the acupuncture points (AP) and outside them. Material and methods. Using the Unna method (polychrome toluidine blue dye), mast cells were detected in the skin. Conducted immunohistochemical study using monoclonal antibodies to neuron-specific enolase and synaptophysin in order to identify neuroendocrine cells. Research results. Analyzed data on the distribution of mast cells in the skin in the area of the acupuncture points in an adult. It was revealed that the distribution of mast cells in the dermis and the hypodermis differs depending on the localization of the acupuncture point. Fat cells take in maintaining homeostasis and regulation of metabolism in the skin. NSE- and synaptophysin-positive cells were detected in the basal layer of the epidermis, in the area of the the muscles that raise the hair, in the area of the hair follicles; in the secretory terminal regions of the sweat glands, as well as outwards from the basement membrane of these regions between the myoepithelial cells. A part of the neuroendocrine cells is in contact with nerve waves. Expression of NSE and synaptophysin depends on AP localization. In AP of the skin of the abdomen and upper limb, a more pronounced expression of NSE and synaptophysin is observed than at the acupuncture points of the skin of the face. The expression of NSE in the structures of the skin in the area of the acupuncture points is more pronounced than the expression of synaptophysin. In the dermis revealed structureless spaces surrounded by mast cells, nerve fibers, blood vessels.

The aim of the present work was to study the development of afferent bonds between GnRH- and monoaminergic neurons in rat fetuses and to identify possible targets affected by LPS-induced inflammation. The innervation was analyzed using retrograde tracing method with DiI dye. At ED17 and ED21 olfactory bulbs (the area of GnRH migration) are innervated with monoaminergic neurons of septum and in lateral hypothalamus. The GnRH- and monoaminergic neuron interaction zones are sensitive to LPS (E. coli) prenatal exposure, which induces pro-inflammatory cytokine synthesis. We suppose that the olfactory bulbs of fetal forebrain can be a possible area of cytokine influence on GnRH- and monoaminergic neuron interaction.

With systemic inflammation, hypoxia, and an increase in the respiratory, a significant increase in the systemic level of pro-inflammatory cytokines is observed. Recently we demonstrated that elevated IL-1β level in blood reduces the ventilatory response to hypoxia. The aim of the present study was to examine the hypothesis that the respiratory effect of IL-1β may be mediating the NO-dependent mechanisms.The experiments were performed on anaesthetized rats. We studied the effects of intravenous administration of cytokine during inhibition of iNO-synthase. In order to we used aminoguanidine bicarbonate - specific inhibitor of iNOS, which was injected in the tail vein for 30 minutes before the administration of cytokine. During the hypoxic rebreathing experiments, was found that the increase of IL-1β level in blood weakens the respiratory response to hypoxia. The ventilatory, tidal volume and mean inspiratory flow responses decreased by 29%, 31% and 53% respectively. INO-synthase inhibitor pretreatment eliminated these respiratory effects of IL-1β. Thus the data indicate that the ability of IL-1β to reduce the ventilatory hypoxic response is mediated by the NO-dependent pathway.

Neuroendocrine tumors (NET) is a heterogeneous group of epithelial neoplasms that develop from cells of the diffuse endocrine system and found in any organ. A distinctive feature of NET is the ability to produce various biologically active peptides and amines. Currently, the most useful markers are the universal marker chromogranin-A (CgA) and specific markers serotonin and 5-hydroxyindolylacetic acid (5-HIAA). The analysis of the clinical significance of the biochemical markers of NETs was carried out by comparative analysis of their levels in serum and urine of 339 NET patients and 66 healthy people. Determination of plasma CgA, serotonin in serum and 5-HIAA in daily urine was performed using standardized ELISA methods using the Chromogranin A ELISA kit (Dako), Serotonin ELISA and 5-HIAA ELISA (IBL) test-systems. The values of CgA, serotonin, 5-HIAA in patients with NET were significantly (p < 0.001) higher than the corresponding control values. Assessment of the diagnostic significance of CgA, taking into account the cut-off level 33 U/l (with a specificity of 98.5%), showed high sensitivity in the general NET group - 80.9%. The serial determination of the marker reflected the effect of treatment. The progression free survival in different treatment regimens for patients with NET has been associated with basal levels of CgA. The medians of serotonin and 5-HIAA levels were maximal in patients with carcinoid syndrome, significantly exceeding the corresponding values in NET patients without clinical manifestations.The data indicate the possibility of using CgA, serotonin and 5-HIAA to improve the accuracy of diagnosis, evaluation of generalization and biological activity of NETs.

Aim of study. To study chemotactic properties of glutamate and glutamate receptor agonists on T cells migration from healthy donors and patients with multiple sclerosis (MS) in vitro. Materials and methods. T cell migration of 15 patients with MS and 15 healthy donors was studied in vitro using transwells. Lymphocytes were activated with PMA (10 ng/mL). T cells were added to transwells with fibronectin (10 μg/mL) pretreated membrane. The lower chamber contained glutamate or AMPA or NMDA (100 μM for each) in complete RPMI medium. Migrated cells were collected and stained with antibodies to CD3-marker for subsequent analysis by cytofluorimetry. Results and conclusion. In presence of glutamate, there is a tendency to a decrease in migration activity in both groups of donors. T-cell chemotaxis of healthy donors, but not MS patients, decreased in concentration gradient of NMDA. The activation of lymphocytes with PMA leads to a decrease in the number of migrated cells by an average of 17% (p < 0.01). In MS patients there is a tendency to an increase in chemotaxis of activated cells in concentration gradient of glutamate, and a decrease with AMPA. Thus, glutamate and glutamate receptors agonists do not possess pronounced chemotactic properties, but rather enhance T-cell migration through synthesis of adhesion molecules on the surface of lymphocytes and endothelium.

The aim of the research was studying the features of neurohumoral regulation of carbohydrate metabolism in experimental diabetes mellitus. A model of diabetes mellitus was created by introducing 0.1% solution of epinephrine hydrochloride into animals. Biochemical parameters of carbohydrate metabolism (cortisol, C-peptide and glucose) were studied in 17 animals on day 0, 15, 21, 30, 45. On the same day morphofunctional changes formed in the pancreas and Nodi lymphatici pancreaticoduodenales were studied. With stress, there is an increase in cortisol and C-peptide and a decrease in the concentration of glucose in the blood. In distress cortisol secretion is reduced, and the production of C-peptide and glucose concentration in the blood increases. In the lymph nodes formed functional changes that led to a violation of cellular and humoral immunity in the body. Conclusion. The cause of diabetes is a failure in the work of self-regulating mechanisms of carbohydrate metabolism, which leads to dysregulation pathology of the autonomic nervous system, manifested by antagonism between adrenaline and cortisol, insulin and cortisol.

Aim. To determine the relationship between the content of nerve growth factor (NGF) and S100b with the clinical manifestations of acute ischemic stroke (IS). Material and methods. A total of 17 patients with IS, age 68.5 (67; 78.5) years were examined; comparison group: 15 volunteers, age 65.0 (62.0; 66.5) years. The patients’ condition was assessed by the size of the brain lesion, the NIHSS and mRS, somatic status. Serum and cerebrospinal fluid (CSF) NGF, S100b, IL6, plasma D-dimer (ELISA) were determined at 1, 3, 10 days after IS. Results. We found NGF decreased in a serum of patients IS with a fatal outcome in 1-10 days. The dependency of serum (r = -0.300, p < 0.05) and CSF (r = -0.271, p < 0.05) NGF with the size of the lesion and patients somatic status (r = -0.322, p < 0.05) was discovered. The concentration of S100b increased from 3 days in deceased patients in the CSF and blood. The S100b correlated with the outcome of the disease (r = 0.650, p < 0.01), NIHSS (r = 0.651, p < 0.01), mRS (r = 0.451, p < 0.05). NGF and S100b levels were associated with the increasing of plasma D-dimer and CSF IL-6. Thus the NGF and S100b reflect the brain damage severity and the patients’ condition in the acute IS and associates with inflammation activity.

The aim of this study was to determine the amplitude-frequency characteristics of the electroencephalogram (EEG) and heart rate variability (HRV) in humans, depending on the initial serum TNF-α level at a single session of heart rate variability biofeedback (HRV BF) due to increase the total power of the HRV spectrum. Among hypertensive individuals (blood pressure 140-160/80-100 mm Hg) subgroups with an optimal serum TNF-α level (below than 75 quartile - 84,4 pg/ml) and with a high serum TNF-α level (more than 84,4 pg/ml) were selected. In individuals with an optimal serum level of TNF-α, an increase in the total HRV spectral power, a decrease in the stress index, systolic blood pressure and a decrease in the EEG power in the theta range in the frontal brain regions after HRV BF session were identified. In individuals with a high serum TNF-α level the effectiveness of HRV BF was minimal against the background of continuing sympathicotonia and high theta EEG-activity.

Comparison of dynamic changes of biochemical reactions in the liver and CNS of freshwater liver mollusc LYMNAEA STAGNALIS has been conducted. It has been conducted during incubation in the highly concentrated solution of glucose. The indicators of superoxiddismutase (SOD) activity, the level of renewed glutation (G-SH), Se-dependant glutation peroxidase (Se-GP) and TBA-active products were estimated and compared. Also for the tissues of the Central Neural System and tissues samples of liver it was found out by glucoseoxidate method the concentration of glucose in haemolymph of the investigated biological object in the conditions of hyperglycemia. A comparative estimation of the general protein concentration in both tissues was conducted. Resistance of the liver tissue to hyperglycemia and a reverse effect towards CNS was found out.

The aim of the work was to compare proteasome mechanisms of the development of donor-specific tolerance (DST) to ovarian allograft in outbred Wistar rats and inbred August rats with the increased level of monoamines and stress limiting systems in the brain. In spite of DST induction in all animals, engraftment was more effective in Wistar rats. In the liver of all rats with survived allograft, the level of proteasome immune subunt LMP2, evaluated by Western blotting, was significantly higher than in control false-operated rats. This difference was more pronounced in Wistar rats. Besides, in the liver of all rats with survived allografts, the level of proteasome PA28αβ activator was higher than in control. In conclusion, the development of DST is connected with the enrichment of liver proteasome pool by immune forms containing LMP2 subunit and PA28αβ activator. This process is partially suppressed in August rats under stress conditions of the central nervous system.

Irritable bowel syndrome, which is a common functional intestinal disorder, can be attributed to psychosomatic pathology, since it contains all three characteristic features of this group of diseases. The study assessed discrimination in the distribution of alleles and genotypes -1082G/A, 819C/T, -592C/A IL-10 in groups of patients with IBS with various psychopathological disorders. The peculiarities of the distribution of alleles and genotypes formed by the polymorphic site -592C/A IL-10 were identified. For groups of patients with “IBS with anxiety disorders” and “IBS with depressive syndrome”, the frequencies of the rare allele and its heterozygous genotype -592C/A were increased. According to the criterion of the odds ratio, prognostic significance was an increase in the carrier frequency only in the group of patients “IBS with anxiety disorders” (OR = 3.9, 95% CI 1.3-12.5). It has been established that the polymorphism -592C/A of the IL-10 gene was associated with the variant “IBS with anxiety disorders”.

The epithelium of the respiratory tract of mammalian lungs contains pulmonary neuroendocrine cells, represented by both single cells and innervated clusters forming neuroepithelial bodies (NEB). Since NEB are intensively innervated and produce highly specific biologically active substances, such as the bronchoconstrictor serotonin, the level of which increases during hypoxia, it is assumed that these structures can play a key role in the pathogenesis of bronchial asthma (BA).The purpose of this study was to the detection and analysis of NEB in the lungs with experimental BA.For the study, we used the lungs of sexually mature Wistar rats (n = 5). NEB was detected by monoclonal antibodies to synaptophysine.It has been found but that in the context of experimental asthma 76.6% NEB were located as part of a simple cuboidal epithelium of small bronchi and respiratory bronchioles. 17.6% of NEB were found in the composition of the epithelial layer and only 5.8% are single NEB in the composition of the epithelium of the small bronchi. At the same time, a greater number of NEB localized in the bronchi were composed of 6 cells (46.2%), 38.5% of 4 cells, and 15.3% of more than 10 cells in one cluster. As in our previous studies, most of the NEB were located in the vicinity of the synaptophysi-immunopositive terminals. Against the background of asthma occurred reduction in the number of large clusters NEB and increased concentrations of medium size of NEB. The results obtained indicate the effect of inflammation on the functional features of the neuroendocrine system of the lungs and the possible contribution of NEB to the inflammatory cascade in BA.

The aim of the study was to elucidate the molecular mechanisms of the interconnection of the GABA-ergic and nociceptive systems at the level of the peripheral division of the CNS. The data obtained indicate that GABA does not affect the activation gating device of the NaV1.8 channel of the primary sensory neuron responsible for coding pain signals.This agent in a wide range of concentrations also does not affect the growth of neurites of sensory neurons of embryonic nervous tissue. These results confirm our assumption, expressed earlier that the asynaptic membrane of the primary nociceptive neuron is not under the control of the GABA-ergic system.

Purpose: to study bone marrow mast cells in mice after autotransplantation. Materials and methods. Mast cells and sulphatedness degree of heparin mucopolysaccharide in the bone marrow were identified using Unna staining with polychromatic toluidine blue. Study results. Data on mast cells distribution in the bone marrow after autotransplantation in 40 minutes and in 2 hours were analyzed. Two types of mast cells’ reaction to autologous bone marrow introduction were identified: sequential degranulation and exocytosis. As a result, secretion of mast cells causes production of biologically active substances in the microenvironment of a mast cell; these substances form chains and conglomerates from granules, changes in the number of which can contribute to changing the process of mitotic division. According to morphological criteria three populations of mast cells were identified: small-sized cells, with blue-colored nuclei stained orthochromatically and located asymmetrically; metachromatic oval-shaped cells with a nucleus located in the centre; large, degranulated, gamma-metachromatic mast cells. Most part of mast cells in bone marrow smears is presented by integral forms. Heparin in mast cells takes part in regulating metabolism in the bone marrow after autotransplantation.

The character, intensity and quantitative indicator (QI) of general nonspecific adaptational reactions (AR) of the body were studied in patients with lung cancer (LC) or biliopancreatoduodenal cancer (BPDC) with various malignant spread. Poor AR characteristics were associated with the presence of metastases, but did not depend on the surgery volume. AR QI significantly differed depending on the metastatic status in patients with resectable LC receiving similar surgery treatment. AR QI in BPDC patients a day after radical pancreatoduodenal resection was higher than after bypass anastomosis. Thus, the studied AR characteristics demonstrated the state of systemic neuroimmune mechanisms of the nonspecific antitumor resistance of the body.

Efficiency of interval hypoxic training in treatment of hypothyroidism with autoimmune genesis in children and adolescents was shown. The therapeutic effect of hypoxic therapy realized not only through amplification of compensatory mechanisms for the oxygen delivery to the tissues, but also through inhibition of humoral immune responses and the stimulation of T-cell immunity in patients with autoimmune thyroiditis. Increase of function and quantity of CD8+-cells after a course of hypoxic therapy prevents the progression of the autoimmune process and helps to restore the function of the thyroid gland, which in turn leads to positive changes in the neurological status of patients: improved mental performance indicators and fine motor coordination. Complications of therapy or deterioration of the patients were not observed. Follow-up monitoring of patients conducted after 6-8 months after treatment showed that the positive effect of hypoxic therapy maintained throughout this period. Positive hormonal and immunological and neurological dynamics in children and adolescents with autoimmune thyroiditis after the interval hypoxic training suggests its inclusion in the scheme of pathogenetic treatment of patients with this pathology.

Recently, the role of the intestinal microbiota in MS has been actively investigated in connection with its influence the development and activity of immune and nervous systems. It is assumed that immune dysfunction, as well as disorders of the gastrointestinal tract and psycho-emotional functions in patients with MS, may be associated with intestinal microbiocenosis dysbiosis. The aim of the study was to assess changes in the intestinal microbiome in MS patients and to analyze the associations of the bacterial level with various subsets of Th cells in the blood and psycho-emotional disorders. 126 MS patients with disease duration of 12.2 ± 0.9 years and 69 healthy individuals were examined. Intestinal microbiome was determined by the Illumina/Solexa sequencing method. The quantitative content of microbial species was determined by the method of cultivation and real time PCR with specific primers, subsets of Th cells - by flow cytometry. Patients were assessed for anxiety, depression, and asthenia. It was shown that the intestinal microbiome of MS patients was significantly changed compared with healthy individuals: the proportion of Bacteroides, especially of the Prevotellaceae family, was reduced, the proportion of Firmicutes (Bacilli and Clostridia) and Actinobacteria was increased, and the symbiotic species in Enterobacteriaceae family were replaced by opportunistic species. A positive correlation between the level of Bifibobacteria spp. with disease severity and blood levels of DP Th17 CM cells. Enterobacter spp. level correlated with the level of “classical” or Th17/22 CM and DP Th17 EM. Bifidobacteria spp. the level was also associated with the level of depression in patients, the level of Escherichia coli and Prevotella spp. - with anxiety, and the level of atypical E. coli and Sutterella spp. - with asthenia. The data obtained suggest that immune and psycho-emotional disorders in patients with MS can be corrected by normalizing intestinal microbiocenosis.

Objective: to study the clinical and immunologica features of the manifestation of chronic pain in systemic lupus erythematosus (SLE) patients with neurological symptoms.Methods. We examined 30 healthy individuals and 38 patients with SLE. Beck’s depression questionnaire was used to assess the presence of depressive symptoms. Antibodies to adenosine deaminase (anti-ADA), β2-glycoprotein-I-dependent antibodies to phospholipids of the IgG class (anti-FL) and antibodies to double-stranded DNA (anti-dsDNA) were determined in the serum of patients with SLE. Doppler sonography of the brachiocephalic arteries was performed for all patients with SLE.Results. Complaints about the presence of headaches of varying severity presented 35 people (92.1%). Migraine was recorded in 63.2% patients with SLE. Doppler ultrasound in patients with SLE with chronic headaches in 66.7% of cases showed signs of reduced blood flow in the arteries of the vertebrobasilar basin, which may indicate chronic brain ischemia. Signs of depressive disorder of varying severity were found in 36.8% of patients with SLE, and in patients with neurological disorders, moderate (p = 0.027) and severe (p = 0.041) depression were more often detected. Elevated levels of anti-ADA were found in 36.8%, and anti-FL in 44.7% of patients with SLE. It was noted that “migraine-like” manifestations of chronic pain syndrome were more common in the group of patients with SLE, who had a combined increase in anti-ADA and anti-FL (χ2 = 4.5; p = 0.024). Since a certain part of ADA is concentrated in the plasma membranes of vascular and platelet endothelium cells, it can be assumed that there is a conformational effect of anti-ADA on the β2-glycoprotein-I, leading to increased synthesis of anti-FL and undesirable activation of coagulation cascade in vessels.Conclusion. The combination of severe chronic headache with high levels of anti-ADA and anti-FL can precede the development of stroke and transient ischemic attacks, which emphasizes the need for additional immunological examination of patients with SLE with neurological symptoms.

Currently the study of the role of peripheral nervous system in control of inflammation in endometriosis and its involvement in the development of the chronic pain syndrome in this pathology is of relevance. The purpose of this work was to assess the reciprocal location of sympathetic and parasympathetic nerve fibers with external genital endometriosis at various stages of progression. The samples for the study were the endometrial biopsies of patients of reproductive age with external genital endometriosis of I-IV stage of the disease, with primary sterility (n = 20). The control group consisted of 3 patients (n = 5) who did not have any signs of endometriosis. Molecular markers were visualized using the immunohistochemical method. Antibodies to tyrosine hydroxylase (TH, 1:200, Abcam, USA) and PGP 9.5 (PGP 9.5, 1:1000, Abcam, USA) were used as primary antibodies. Alexa Fluor 488 (1:1000, Abcam, USA) and Alexa Fluor 647 (1:1000, Abcam) were used as secondary antibodies. The results were visualized with a confocal microscope (FluoView1000 (Olympus)). 3D shooting was used to assess the reciprocal location of the studied markers. As a result of this work, it was found that the expression of both of studied markers was detected in all samples. The obtained data can significantly increase the understanding of the functioning mechanisms of the neoneurogenesis processes in ectopic and eutopic tissue, thereby allowing an increase in the accuracy of the endometriosis diagnostic methods.

The article presents the results of a comprehensive analysis of the parameters of innate and adaptive immunity in 85 patients with recurrent remitting multiple sclerosis (MS) with its exacerbation (54 people) and in conditions of persistent clinical remission (31 people). It is shown the signs of autoinflammation and increased reactivity of the T-link of adaptive immunity to be registered not only in exacerbation, but also in remission. The revealed changes determine the pathogenetic basis of MS progression and they should be taken into account when accompanying patients in remission to prevent clinical activation.

Objective: Based on the study of some indicators of cellular and humoral immunity, evaluate the features of immunoreactivity in patients with psoriasis with concomitant pruritus. Materials and methods. Patients were examined with vulgar PS (n = 97), which were divided into 2 groups: group 1 - PS with pruritus (n = 73, mean age 40.0 ± 1.5 years), group 2 (comparison group) - PS without pruritus (n = 24, mean age 41.5 ± 2.7 years). The cellular immunity indicators was carried out by flow cytofluorimetry. Phagocytic activity of peripheral blood neutrophils was studied microscopically by the absorption of latex particles. Concentrations of immunoglobulins, cytokines, circulating immune complexes in the blood serum were evaluated by the method of enzyme-linked immunosorbent assay. Statistica 6.0 was used for statistical analysis. Our studies allowed us to identify features of PS with concomitant pruritus: severe clinical course of the disease with damage to the musculoskeletal system, associated with selective deficiency of class M immunoglobulins and increased activity of phagocytic neutrophils.

Impairments of immune system are an important mechanism of the degenerative dystrophic processes in the arthral tissues onset and development.The objective of this research was to study the cellular immunity condition in patients with osteoarthrosis before and after endoprosthesis implantation. The research methods included immunophenotyping of lymphocytes in the peripheral blood. The immunologic impairments before the surgery referred to change in T-cell immunity reflecting in the imbalance of immunoregulatory subpopulations (decrease of T-suppressor level and increase of T-helper content). At that the number of NK-cells rose which didn’t exclude a possible connection with the cartilage tissue degradation impurities on the background of B-cell number decrease. During the post-surgery period the decrease in T-helper and T-suppressor numbers was detected which may be related to their migration to implantation area due to the decrease of their number in the systemic circulation, at that no significant changes in T-lymphocytes were observed. By contrast, there was a decrease of NK-cell number at higher level of B-cell number showing an adequate response of the bodies for surgery aggression. The results of immunological research are worth being taken into account when preparing patients for endoprosthesis implantation surgery for the purpose of prescribing the immune-correcting drugs for pre-existing impairments of cellular immunity as well as in the post-surgery period to relieve the effects of surgical interference aggravating the impairments in this population of patients.

The purpose of the study was to identify the dependencies between the content of cytokines, neuronal antibodies and changes in the bioelectrical activity of the brain in patients with neurointoxication with mercury, depending on the severity of the pathological process. Surveyed men with professional chronic mercury intoxication I-II degree - 17 people and 33 - with ChMI III degree. The serum ELISA was used to determine IL-1β, IL-4, IL-8, IL-10, TNF-α, INF-γ, and AT to nerve tissue proteins (NF-200, GFAP, S-100, MBP, MAG, B-end. Ca-canal, B2GP, DNA, Glu-R, GABA-R, DA-R, Ser-R, AH-R). Visual evoked potentials were evaluated on an electroencephalograph. As a result of the research, the peculiarities of the relationship between cytokines and neuronal antibodies, indicating the initiation or regulation of immunopathological reactions depending on the degree of ChMI, were revealed. When ChMI I-II Art. IL-1β hyperproduction was accompanied by an increase in AT to Ser-R, B-head Ca-channel and a decrease in AT to Glu-R. In patients with ChMI III degree a decrease in IL-1β is associated with increased production of antibodies to S-100, and a decrease in TNF-α with increasing antibodies to NF-200, GABA-R, GFAP. In patients with ChMI with high levels of antibodies to S-100, a more pronounced delay in the appearance of the response of the cortex to the visual stimulus, an increase in the latency of P200 was revealed. Thus, the obtained data confirm the complex functional relationships between the nervous and immune systems, the selectivity and selectivity of damage to the structures of the nervous tissue at various stages of ChMI, which can serve as unique biomarkers.

Bronchial asthma is a classic, antigen-specific disease, the formation of which is crucial reagin-dependent type of allergic reaction. However, the interaction of changes in the immune status and bioelectrical activity of the brain in patients with bronchial asthma is currently insufficiently covered. The paper analyzes the interdependence between changes in the immunological reactivity and bioelectric activity of the brain in patients with bronchial asthma. Changes in the immune state during bronchial asthma led to the development of hypoxia, which had a significant impact on the bioelectric potentials of the brain, manifested in the predominance of the alpha rhythm, left hemispheric dominance of alpha power in the anterior temporal leads.

The aim of the work is to study the level of systemic inflammation and changes in adaptive immunity in the early period after acute psychosis to assess their participation in the pathogenesis of alcoholic mental and cognitive disorders. We examined 28 patients with alcoholic psychosis (AP) and a control group of 17 healthy volunteers. Indicators of systemic inflammation and immunity, including key cytokines and lymphocyte subpopulations, were investigated. After acute psychosis of patients with alcoholism, pronounced activation of humoral immunity with impaired clearance of immune complexes, increased content and activity of Th2 with signs of insufficiency and dysfunction of Th1, reduced content and activity of cytotoxicity system cells and signs of systemic inflammation (increased CRP, cortisol, cytokines). Activation of Th2 response and an excess of proinflammatory mediators in patients with AP through various ways of interaction with the Central nervous system (n. vagus, choroidal plexus of the ventricles, and others) can participate in the disorders of metabolism of neurotransmitters in the Central nervous system involved in the pathogenesis of alcoholism, and in the maintenance of neuroinflammation. A high level of systemic inflammation can be both a trigger of psychosis and a manifestation of violations of neuroimmune interactions, as well as the development of excitotoxicity and damage to neurons in acute psychosis.

The aim of the work was to study the factors of natural and adaptive immunity and systemic inflammation in subacute stage of schizophrenia to clarify the role of these systems in the chronization of the disease. 31 patients with the diagnosis of schizophrenia (SCI) with paranoid after 3-4 weeks of therapy were examined. The control group included 16 healthy volunteers. Markers of systemic inflammation and immunity, including key cytokines and lymphocyte subpopulations, were investigated. Increased levels of IgМ, C-reactive protein and cortisol in the blood were found in patients with SCI. Also in most cases the content of proinflammatory proteins IL-8, IL-6 and IL-10 was increased. The greatest increase in the levels of systemic inflammation and cytokines was found in patients with first psychotic episode. The content of HT was more often normal, but the level of NT-4 and nerve growth factor β (NGFβ) in most patients was positively associated with levels of IL-6. At low levels of BDNF a significant increase in levels of CIC, cortisol, IL-8, IL-6 and IL-10, but not Ig were found. Also, in patients with low BDNF symptoms of delusions prevailed, while in cases of normal or elevated BDNF (19 out of 24 cases), in addition to delusions, hallucinations were pronounced. Conclusion. It is believed that antipsychotic drugs reduce systemic inflammation and activity of the immune system. However, we have found signs of severe systemic inflammation, activation and dysfunction of the immune system in patients with SCI after 3-4 weeks of therapy. Preservation of immune disorders and systemic inflammation in patients with SCI despite clinical improvement can participate in the progression of the disease through neuroimmune interactions. Further studies of the trigger mechanisms of chronic immune activation are needed.

According to statistics, approximately 75-80% of cases of diabetes mellitus in women during pregnancy show the presence of a urogenital infection in which the development of the inflammatory process is conducive to the elimination of the pathogen and the appearance of necrotic tissue. Such inflammatory processes, as a rule, occur with the participation of macrophages attracted by B-lymphocytes and NK-cells. The main goal of this study was to evaluate the expression ratio of immunocompetent cells: macrophages, NK cells and B lymphocytes in the placenta in women with diabetes mellitus who are in different age groups. Molecular markers were visualized using an immunoistochemical method. Were used antibodies to CD68 (1:300, Dako, USA) for macrophages, CD20 (1:300, Dako, USA) for B-lymphocytes and CD57 (1:300, Dako, USA) for natural killer cells. The results were visualized on a confocal microscope (FluoView 1000 (Olympus)). For scoring of microphotographs program “Morphology 5.2” was used. On the microphotographs the relative area of expression was evaluated, signified as the ratio of the area of the immunopositive reaction to the total area of the slide and the optical density. Then a statistical evaluation of the obtained data in the “Statistic 10.0” program was carried out. During the experiment, a sharp decrease in the expression of the CD68 marker in the placenta was detected. A decrease in the expression of the CD20 marker with an increase in the age of patients with diabetes mellitus was also demonstrated, while in healthy women an increase was observed in the middle age group. For natural killers, there was no difference between healthy and sick women. The result indicates a weakening of the reaction of the immune system in diabetes mellitus.

In the present study, an analysis of cognitive, behavioral, and metabolic changes during the dynamics of the development of pathology was conducted under an experimental model of chronic fatigue syndrome (CFS). A decrease in physical and research activity of experimental animals indicated the development of fatigue and a depressed emotional state. An increase in the concentration of lactate was also showed, that may indicate a violation of the energy metabolism.

The aim of this study was the identification of the neuroimmune mechanisms of cognitive impairment on the basis of investigation of an of cognitive disorders association with functional activity of blood mononuclear cells and the synthesis of tumor necrosis factor - α (TNF-α) in patients with affective disorders in the form of depressive reactions and depression.TNF-α expression level in blood mononuclear cells of patients conducted with using the reverse transcriptase polymerase chain reaction method. The proliferative activity of blood mononuclear cells was investigated by a standard method based on the inclusion of a radioactive label. Cognitive function was assessed on the basis of perception, memory, praxis, speech, and control function. The severity of affective symptoms was measured by the Hamilton scale. It was found that patients with depressive reactions were characterized by the mild non-elemental cognitive impairment; while, in patients with depression, more severe non-elemental cognitive impairments in the form of decreased attention, memory, and daily activity were observed. In patients with affective disorders in the form of depression, an increase in the synthesis of TNF-α in blood mononuclear cells was detected, both an increase of the expression frequency of its gene and an increase in mRNA level, as well as an increase of the proliferative activity of blood mononuclear cells, which indicates the presence of immune system dysfunction in this category of patients.Thus, in patients with depression, activation of the TNF-α synthesis in blood mononuclear cells occurs: an increase in the frequency of its expression and an increase of the level of mRNA; these changes are accompanied by the increasing of immune cells functional activity and moderate non-delicate cognitive disorder in the form of cognitive impairment.

In order to investigate the function of human endogenous retrovirus HERV-E λ 4-1 in multiple sclerosis pathogenesis, the comparative research of frequency of this retrovirus expression and mRNA level on different types of blood immune cells of progredient course multiple sclerosis patients have been conducted with using of the reverse - transcriptase polymerase chain reaction method. Peripheral blood mononuclear cells were isolated on Ficoll density gradient centrifugations. Monocytes were separated by the adhesion to plastic Petri dishes. For the estimation of the mitogen-induced HERV-E λ 4-1 expression, blood mononuclear cells were incubated with adding of phytogemagglutinin or pokeweed mitogen during 72 hours in CO2 incubator at 37 °C and 5% CO2. Results of HERV-E λ 4-1 env gene expression estimation demonstrate that both monocytes and lymphocytes express HERV-E λ 4-1. The level of the HERV-E λ 4-1 env mRNA was higher in lymphocytes than in monocytes. The main source of HERV-E λ 4-1 in progredient course MS patients between blood immune cells are lymphocytes, especially B lymphocytes.

The present experimental study aimed to find the most informative peripheral cellular-molecular immune markers, which can determine a risk of the development of Parkinson’s disease. The experiments were performed in transgenic mice of the A53T strain (2 months) characterized by an increased expression of alpha synuclein and genetically predisposed to Parkinson’s disease during aging. In comparison with the WT strain mice (control), A53T mice were found to have a reduced emotionality (increased horizontal motor activity and a significant decrease in defecation acts in the open field test) along with unchanged coordination and balance, tested using the Rotarod + hardware-software complex. These mice were also characterized by significant changes in the content of immune cell subpopulations in the peripheral blood - an increase in the percentage of CD3+T cells and CD3+4+T helper cells, a decrease in the content of CD19+B cells, with unaltered numbers of CD3+4+25+ 27-regulatory, CD19+25+B-regulatory cells and CD11b+115+monocytes. The percentage of T-regulatory cells expressing Toll-like receptors of the 2nd and 4th types (TLR2 and TLR4) was higher in A53T mice than in controls, while the number of cells expressing only TLR4 was reduced. The TLR2 expression did not differ between A53T and control mice. Analysis of the TLR2 and TLR4 expression on CD11b+115+monocytes has shown that the percentage of these cells with TLR4 was reduced in A53T mice compared to the control, while the content of cells with both TLR types did not depend on genotype. Proinflammatory cytokines (IL-6) prevailed over antiinflammatory (IL-10) in the supernatant of mononuclear blood cells of A53T mice suggesting the development of neuroinflammation.The study was supported by Russian Foundation of Basic Research (grant N18-015-00226 А).

Alzheimer’s disease (AD) is the most widespread neurodegenerative disease of older age, which is associated with the deposition of amyloid-beta polymerized peptide (consisting of 42 amino-acid residues) in the brain. The microglial phagocytosis disturbance, which is observed during AD, is possibly the key factor in the process. The research of neutrophils in patients with AD is of special interest due to the pressing problem of finding peripheral markers of AD. Analysis of neutrophils’ functional state in patients with AD is the objective of the present study. A reliable decrease of neutrophils’ phagocytic activity was established in group of patients with AD in comparison with control group (p < 0,05) (PI = 1.16 [0.64; 2.68] and PI = 2.34 [2.06; 2.85], respectively). A reliable increase of leukocytic elastase (LE) enzymatic activity (p < 0.05) was discovered in neutrophil lysate in AD group compared to control (LE = 0.43 [0.29; 0.77] and 0.29 [0.26; 0.38], respectively) at the same time. Comparison of PI and LE indicators in neutrophils’ lysate of AD group showed negative correlation between these parameters (r = 0.49, p < 0.05), which means that phagocytosis reduction during AD is accompanied by simultaneous LE activity increase in lysate of these cells.The obtained results allow to draw a conclusion that neutrophils’ phagocytic activity decreases during AD. Thus, discovered changes in neutrophils’ functional state can be considered as a potential peripheral AD marker.

An important parameter of scaffold matrices is biocompatibility. Biocompatibility assessment is carried out in several stages. At the first stage, its compatibility with in vitro cell cultures is determined. At the second in vivo stage, biocompatibility is assessed by examining histological preparations of tissue biopsies obtained from the area of implantation of scaffolds in experimental animals. Therefore, the following tasks are set: to determine the immunological compatibility of the blood cells of rabbits during the surgical introduction of scaffolds and to evaluate the nervous stress during operations. In our studies, the pcl scaffolds presented are polymeric biodegradable matrices that are polycaprolactone and polyhydroxybutyrate. Capsules consist of polypeptides and polysaccharides, the shell of which is coated with a layer of silicate nanoparticles.

The goal of this research was to study the clinical efficacy of course-based neurotrophic therapy in mild cognitive impairment (MCI) and the effect of therapy on immune parameters in patients, and to assess the prognostic value of the dynamics of immune parameters during the year after treatment. 20 patients with MCI receiving intravenous Cerebrolysin (20 infusions of 30 ml with increasing dose during the first four days) were examined. Neuropsychological and immunological examination was carried out immediately before the study, after 3 months., 6 months and after 1 year after the end of treatment. It was found that after therapy, patients had a long-term decrease in the severity of systemic inflammatory response, and that marked signs of systemic inflammation at the beginning of follow-up combined with a persistent decrease in the level of immunoglobulin G in dynamics were prognostic markers of MCI progression. In conclusion, it wass shown that neurotrophic therapy has a good clinical effect and has a favorable immunomodulatory effect in aMCI, and the relationship between the dynamics of humoral immunity and systemic inflammation and the risk of progression of cognitive impairment in patients within 1 year after therapy was established.

Using flow cytometry and real-time RT-PCR, we studied the effect of the blockade of glutamate NMDA receptors on the quantitative distribution of IFNγ- and IL-4-producing CD4+ and CD8+ T-lymphocytes and the expression of transcription factor of genes T-bet and GATA-3 in immune cells derived from healthy individuals and multiple sclerosis patients (MS). From the results of the study, it follows that blockade of NMDA receptors leads to a decrease in the proportion of studied effector subpopulations of T-lymphocytes, as well as differential modulation of gene expression of transcription factors (TBX21, GATA3). The severity of the negative effect of receptor blockade differs in different subpopulations of CD4+ and CD8+ T cells, which leads to a shift in the cytokine balance towards “proinflammatory” type 1 T-cells, to a greater extent in patients with MS. Thus, glutamate can regulate the Th1/Th2 and Tc1/Tc2 сytokine balance by modulating the activity of NMDA receptors of T lymphocytes in MS.

Inflamm-aging - the term, describes the development of chronic inflammation during aging without the infection pathology. It is supposed, that inflamm-aging is one of the reason of age-related pathology, partially, Alzheimer disease (AD). There were done comparative analysis of AD (Аβ42, τ-protein, р16) and inflammation (IL-6, TGFα, NF-kB) markers in hippocamp and blood lymphocytes in elderly and old people. It was shown, that expression of investigated signal molecules in hippocamp and lymphocytes of elderly and old AD people increased in comparison with people of control group (without neurodegenerative pathology). Thus, inflammation mediators play important role in AD pathogenesis and can be the potential target for neuropathology therapy.

The hypothalamic orexin system is critically involved in addiction, including chronic alcohol abuse. Microinjection of orexin into the lateral hypothalamus increases alcohol intake in rats, while reduced immunoreactivity of orexin neurons is associated with decreased alcohol drinking. Recently, the numbers of orexin neurons were found to be increased in opiate addiction in humans [4] and cocaine addiction in rats [2], but the integrity of orexin neurons has not yet been studied in human alcoholics. We examined the hypothalamus of 9 patients of chronic alcoholism and 10 subjects without a history of alcoholism or any other neurological or psychiatric disorder. We performed immunohistochemistry for orexin A, followed by stereological quantification. The hypothalamic tissue of chronic alcoholics exhibited a slightly increased number (9%) of orexin-containing neurons compared to the control group (123’087 ± 18’536 and 110’431 ± 14’439, p = 0.11). Mean Gundersen’s coefficient of error was 0.06 ± 0.01. The number of orexin neurons was similar in chronic alcoholics and control subjects without a history of alcoholism. Further examination of alcohol-induced hypothalamic damage is needed to understand, whether a neuroplastic increase in orexin neurons counterbalances a concurrent alcohol-toxic damage to these neurons.

Parkinson’s disease (PD) is a neurodegenerative disease characterized by α-synucleinopathy, which involves all districts of the brain-gut axis, including the central, autonomic and enteric nervous systems. Previous findings suggest that the intestinal microbiome is altered in PD and is related to motor phenotype. However how dysbiosis arises and whether this feature contributes to PD pathogenesis remains unknown. The aim was to evaluate gut microbiome and the serum cytokine profile in PD. We quantified serum interleukin (IL) levels (IL-1β, IL-6, IL-10, TNF-α, IFN-γ) in 55 PD patients. Study of the fecal samples was performed by real time PCR method and bacteriologically. Discovered the relationship between the intensity of dysbiosis and the level of proinflammatory cytokine IFN-γ, IL-6.We show that disturbances in plasma cytokine level could be more profound in PD patients with altered composition of intestinal microbiota, which may explain the mechanism of influence of microbiota composition on the PD manifestations.