Репозиторий Университета

© 2018, Bionika Media Ltd. All rights reserved. Objective. To carry out a systematic analysis of the data available in the literature on rational therapy for vaginal microbiocenotic disorders during combined antibacterial therapy to optimize the use of probiotics. Material and methods. The review includes the data of foreign and Russian articles found in the international system Pubmed. Results. The polymicrobial etiology of the inflammatory process requires combined antibacterial therapy using 2–3 antibiotics, which predisposes to dysbiotic states and the growth of opportunistic pathogens, including Candida fungi. It is advisable to prophylactically take probiotics simultaneously with the initiation of antibiotic therapy, which is more effective than the use of probiotics immediately after completion of an antibiotic therapy cycle. The vagina can be colonized by probiotic bacteria following oral administration if acid-resistant strains of lactobacilli are used. Conclusion. It is expedient to simultaneously take acid-resistant probiotic strains per os during antibiotic therapy in order to restore a normal protective flora and to suppress the opportunistic intestinal microorganisms that are able to colonize the urogenital area.

© 2018, Dynasty Publishing House. All rights reserved.  Objective: to evaluate the possibility of creating a human model of acute Helicobacter pylori infection in healthy volunteers after infecting them with a mutant rifampicin-resistant strain of H. pylori KM-11 (Rif R ), to obtain evidence of H. pylori survival and invasion into the gastric mucosa, describe the symptoms, and assess the efficacy of H. pylori eradication therapy with Stimbifid plus. Materials and methods. In our experiments, we used conventional white mice of both genders weighing 18–20 g. The concentration of bifidobacteria, lactobacilli, and Escherichia (CFU) in animal faeces was determined by inoculating tenfold dilutions of biomaterial onto solid media and further counting of bacterial colonies grown after the incubation period. Microorganisms were cultivated in an anaerobic incubator and then identified by morphological evaluation and using biochemical identification kits. We created a murine model of H. pylori infection by oral administration of H. pylori KM-11 (Rif R ) suspensions to immunocompromised mice that had earlier undergone intramuscular administration of dexamethasone. For a human model of H. pylori infection, we selected healthy male volunteers. They took suspensions of H. pylori KM-11 (Rif R ) isolates in isotonic sodium chloride solution. Fecal specimens were collected from volunteers on daily basis during the entire follow-up period and then 2 weeks and 1 month after treatment completion. Fecal suspensions in isotonic sodium chloride solution were inoculated onto the selective hemin-containing solid media with rifampicin at a concentration of 160 µg·mL –1 . The results of this experiment (H. pylori colony count) were used to evaluate the efficacy of H. pylori eradication therapy with Stimbifid plus. Results. Both in vitro experiments and murine models demonstrated high anti-H. pylori activity of Stimbifid plus and its ingredients, restoration of the gastric microbiota, restoration of gastric colonization resistance, and eradication of H. pylori KM-11 (Rif R ). Self-infection with H. pylori KM-11 (RifR) caused acute infection in volunteers. The disease manifested with mild ailment, epigastric discomfort, belching, increased stool frequency, and changes in the color of stool. The detection of H. pylori KM-11 (Rif R ) in the faeces of volunteers and isolation of pure cultures prior to treatment initiation indicated bacterial adhesion to gastric mucosa and survival of microorganisms. Treatment with Stimbifid plus caused gradual decrease in the number of bacteria isolated from feces and their complete elimination by day 11 of therapy. All fecal specimens collected 2 weeks and 1 month after therapy completion from volunteers were negative for H. pylori KM-11 (Rif R ). None of the study participants required in-patient treatment. Conclusion. The results of our experiments obtained in both murine and human models of H. pylori infection will be used for more detailed assessment of this pathological process, clinical manifestations, impact of H. pylori virulence factors on the host, choosing new methods for the prevention and treatment of chronic gastritis caused by H. pylori, and monitoring the efficacy of eradication therapy.

© 2018, Bionika Media Ltd.. All rights reserved. The authors have established a relationship between intraepithelial cervical lesions and vaginal biocenotic disorders in pregnant women with human papillomavirus (HPV) infection and determined their management tactics. The HPV–positive pregnant women have a high incidence of vaginal dysbiosis (38.7%) that is, in most of them, characterized by co–infection (65%), mainly by anaerobic and aerobic infections (44.1%). High-rate HPV in the pregnant women is associated with bacterial vaginosis, mixed dysbiosis, and their recurrences and with the frequency of atypical squamous cells of undetermined significance (ASCUS) and low-grade squamous intraepithelial lesions (LSIL) in the presence of an inflammatory response. Restoring the normal microflora contributes to the disappearance of the inflammatory response and to the reduction of ASCUS. Therapy for dysbiosis does not change the rate of LSIL at 3-month follow-up.

© 2018 Bentham Science Publishers. Background: This study discusses the crucial factors responsible for the progression of atherosclerotic cardiovascular disease (CVD). The interaction between the gut microbiota, heart and vessels in CVD pathogenesis is extremely complex and includes components such as direct bacterial translocation from the gut to vessels and metabolitemediated damage. To a greater extent, CVD seems to be entangled with a subtle immune system-to-microbiota interface. From among the most significant advances in recent years in this area, it is necessary to highlight the discovery of the pro-atherogenic effect of trimethylamine-N-oxide (TMAO) and changes in the activity of effector T-cells in the settings of dysbiosis. Currently, we are witnessing an explosive growth in interest in using the microbiota and interlinked cascades as a target for therapeutic interventions, including direct microbiome targeting, the attenuation of toxic metabolite-induced damage, the modulation of intestinal immunity, and downstream inhibition of systemic inflammatory pathways. Objective: In this brief review, modern strategies of microbiome-based therapies for the prevention and treatment of CVD are classified and discussed from the perspective of personalized medicine.