Abstract. The paper represents a synopsis of current publications concerning existence of free extracellular DNA. Such DNAs are not associated with cells of the organism, being revealed in nearly all body fluids. Recent data show that the cell-free DNA is determined in normal, healthy organism as well. Increased level of free DNA plasma and serum are detectable in many diseases, including autoimmune disorders, malignant neoplasias, myocardial infarction, etc. In many cases, free DNA may be suggested as predictive markers for various distinct diseases, as well as worsening of their clinical course. Physiological role of free DNA is not yet clear, like as its importance in development of certain diseases. It was shown that free DNA may exert stimulatory or suppressive effects upon functions of immunocompetent cells. Free extracellular DNA may also perform an inducing role for autoimmune conditions. In addition, one may assume that free DNA may be a carrier of genetic information in the body between tumor and normal cells in the body, like as between normal cells in various organs and tissues.

Abstract. There are some specific mechanisms in cell that detect the invasion into the cell of any foreign molecules, so-called pathogen-associated molecular patterns (PAMPs). The recognition of these PAMPs is realized by Toll-like receptors or is due to the cytosolic sensors action. In recent years much attention is directed to the investigation of foreign nucleic acids sensing and detection in cell. Nowadays some sensors of doublestranded DNA, such as STING, DAI, members of NOD-like protein family, RIG-like helicases, proteins of HIN-200 family are identified. Some of sensors interact with double-stranded DNA directly. The others are characterized as mediators of signal transduction from unknown DNA-sensor in the series of following molecular events. Induction of nuclear transcription factors NF-κB and IRF3/IRF7 to produce IFNβ or processing of proinflammatory cytokines IL-1β and IL-18 by means of inflammasome formation is a result of activation of cascade events induced by cytosolic DNA. In the review we combine information concerning signaling pathways characterized sensing of intracellular double-stranded DNA that results in the development of the cellular immune response.

Abstract. This study has shown detectable production of IL-8, as a fraction of cytokine pool induced in culture of human peripheral blood cells (PBCs). Mean amounts of IL8 produced in presence of γ-globulin fraction proteins and/or their metal complexes with zinc ions varied from 575.0±27.77 to 6355.0±480.98 pg/ ml. The complexes of γ-globulin with zinc (48 h of culture) caused increase of IL-8 production that was 1.8-fold higher than with control γ-globulin and 1.4-fold higher than with of zinc ions alone (p < 0.02). Dynamic tracking of the cytokine levels has shown that PBCs induced with γ-globulin/metal complexes produced IL8 as a factor of prolonged or late-type response.

Abstract. Complicated systemic inflammatory response syndrome in patients undergone open-heart surgery is an important issue of cardiac surgery. The conditions and trigger mechanisms leading to such a complication remain unclear.

We studied the impact of mechanincal myocardial injury products released into blood during open-heart surgery, lipopolysaccharides and their combination on isolated monocytes.

It was found that mechanically injured myocardial tissue can be a source of intracellular heat shock protein 70 (Hsp70). The content of Hsp70 in the cytosolic cardiomyocyte fraction responsible for mechanical myocardial injury modeling corresponds to the level of proinflammatory cytokine production by monocytes and the density of TLR4 surface expression. The study results confirm the synergy and potentiation of the combined impact of mechanical myocardial injury products and lipopolysaccharides on the levels of cytokine production by monocytes.

Abstract. During the passage through the utero-placental circulation, peripheral blood monocytes are exposed to action of various soluble placenta-derived factors. Subsequently these cells migrate to placental tissue and play a key role in regulation of placental growth and development. We investigated the influence of placental secretory factors upon expression of THP-1 cells surface receptors during normal pregnancy, and pregnancy complicated with preeclampsia. Soluble placenta-derived factors produced by the third-trimester placenta caused reduced intensity of CD11а, CD18, CD54, CD14, TRAIL and VEGFR1 expression on THP-1 cells, as compared with the first-trimester placental extracts. Soluble placenta-derived factors from preeclamptic placenta caused an increased intensity of CD18 and CD54 expression by THP-1 cells and decreased intensity of VEGFR1 expression in comparison to normal pregnancy. The work was supported by grants of the President of the Russian Federation № НШ-131.2012.7, СП-3492.2013.4 МК-1580.2013.7 and by grant РФФИ № 13-04-00304 А.

Abstract. Enhanced transendothelial migration of leukocytes during infection and inflammation occurs due to increased expression of ICAM-1 and VCAM-1 adherence molecules of the immunoglobulin superfamily, and increased secretion of chemokines by endothelial cells. Our previous in vitro studies with human monocytic THP-1 cells showed that some components of Streptococcus pyogenes caused a sufficient enhancement of transendothelial cell migration. However, expression levels of adhesion molecules remained unchanged on endothelial cells. The purpose of the work was to study mechanisms underlying the enhanced transendothelial migration of THP-1 cells treated with supernatante of streptococcal cells (SSC). SSC exhibited chemoattractive activity towards THP-1 cells. SSC increased chemotaxis and transmigration of THP-1 cells. Meanwhile, a 24-hour preincubation of THP-1 cells with SSC caused suppression of the both effects, being accompanied by decreased level of Focal Adhesion Kinase phosphorylation. Preincubation of THP-1 cells with pertussis toxin did reduce the transmigration intensity in presence of the SSC down to the level of spontaneous migration. These results suggest that increased transmigration of THP-1 cells under the influence of SSC may be determined by its chemoattractive action upon the migrating cells.

Abstract. The article deals with biological issues of obesity, a global epidemic of XXI century. Adipose tissue is considered not only an energy-storage tissue, but as an endocrine organ as well which secretes a variety of bioactive substances (adipokines) including tumor necrosis factor (TNF)-α, interleukin-6 (IL-6). Cardiovascular diseases represent the main cause of morbidity and mortality in persons with excessive weight and obese patients. Atherosclerotic lesions represent a pathological substrate of these illnesses. The aim of our study was to analyze corelations between some specific adipocytokines (such as leptine) and some nonspecific cytokines (such as IL-6, TNFα) with indicators of lipid and carbohydrate metabolism. The study group included 123 persons (100 subjects with overweight and obesity, 23 persons with normal weight).

The article present results of studying immune parameters of patients with obesity, including cytokine levels, major classes of immunoglobulins, lymphocyte subpopulations in blood serum, and their interrelations with disturbances of carbohydrate and fat metabolism.

Abstract. Present study was aimed to perform a quantitative determination of B lymphocyte subpopulations, i.e., B1, B2, memory B cells and CXCR3-positive B cells in peripheral blood of nineteen patients with chronic hepatitis C (HCV) and thirty-two healthy blood donors. Phenotyping of B cell subsets was performed by means of flow cytometry, using a combination of specific monoclonal antibodies, i.e., CD5-FITC/CD27-PC7/CXCR3-APC/CD19-APC-AF700/CD45-APC-AF750. Total numbers of B-lymphocytes and their subpopulations in peripheral blood of HCV-infected patients did not differ from appropriate values in control group. Meanwhile, expression of CXCR3 chemokine receptor in HCV patients proved to be significantly increased in all subsets of B cells. These results suggest a possible involvement of CXCR3-positive B cells into pathogenesis of chronic HCV infection.