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Introduction. Preeclampsia (PE) is a serious complication of pregnancy that occurs in 3-8% of pregnant women and is the leading cause of maternal and perinatal morbidity and mortality.Aim. To evaluate the role of vascular homeostasis gene polymorphism in the formation of preeclampsia.Materials and methods. The sample for this study included 250 women with preeclampsia and 209 women with normal gestation (control group). Five polymorphic loci of vascular homeostasis genes were selected for analysis: α-adducin (G460W ADD1), β2-adrenoceptor (+46G/A ADRB2), endothelin-1 (Lys198Asn EDN1) encoding the β3 G protein subunit (G/A GNB3), cytochrome 3A5 (+6986G/A CYP3A5). The molecular genetic study of all SNPs was carried out by polymerase chain reaction.Results. It was found that genetic variants determine the  risk of  developing preeclampsia. The allelic variant 198Lys EDN1  (84.80%) occurs in  women with a  clinical diagnosis of  PE significantly more often than in  women of  the control group (79.67%) (p = 0.05; OR = 1.43; 95%CI 1.01–2.03). At the same time, among pregnant women without PE, combinations of 198Asn EDN1 x +46 A ADRB2 (23.65%) and 198Asn EDN1 x 460 ADD1 x +46 A ADRB2 (23.65%) are registered 1.6–1.7 times more often than among women with PE (14.46 and 13.65%, respectively, рperm = 0.032). Conclusion. The risk factor for the formation of preeclampsia is the 198Lys EDN1 allele (OR = 1.43), and combinations of genetic variants 198Asn EDN1 х +46 A ADRB2 (OR = 0.55) and 198Asn EDN1 х +46 A ADRB2 х 460G ADD1 (OR = 0.51) have a protective value.

Over the past two decades, active study of the microbial ecosystem of the host organism gastrointestinal tract has led to the recognition of gut microbiome as a "key player" that carries a significant immune pressure and is responsible both for the course of physiological processes and for the development of pathological conditions in humans and animals. A vast number of bacteria living in the human gastrointestinal tract are considered as an organ functioning in dialogue in formation of immunological tolerance, the regulation of normal functional activity of the immune system and maintaining the intestinal mucosa homeostasis. However, disturbances in interaction between these physiological systems is closely related to the pathogenesis of different immune-mediated diseases. In turn, in a large number of works chronic social stress, along with the use of antibiotics, pre- and probiotics, is recognized as one of the leading factors modulating in the microbiota of the gastrointestinal tract. This review focuses on the role of the gut microbiome in the regulation of immune responses of GALT under stress and modulation of its composition by antibiotics and probiotics administration.

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Chronic social stress (CSS) can cause physiological disturbances, provoking the development of depression and anxiety, and stress induced immune dysregulation is a trigger for the development of many pathological conditions, including inflammatory bowel diseases. New data in human and animal models suggest an intriguing relationship between endoplasmic reticulum stress, depression and inflammation. Under cellular stress, the number of protein folding disorders increases, which leads to the development of endoplasmic reticulum stress (ERS). The ERS, in turn, activates the "unfolded protein response" system (unfolded protein response, UPR), the IRE1-XBP1 signaling system is very important. The transcription factor XBP1 is responsible for regulating the expression of a large number of genes involved in the proper folding and maturation of proteins, the degradation of misfolded proteins and regulation of immune responses. In addition, changes in XBP1 expression can significantly affect the risk of developing the disease and the progression of inflammatory and autoimmune diseases, including inflammatory bowel disease.