Репозиторий Университета

© 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.