Peptic ulcer of the stomach and duodenum is a chronic recurrent disease that occurs with alternating periods of recrudescence and remission. The main manifestation of this disease is the formation of a defect in the wall of the stomach and duodenum. One of the main factors in the occurrence of peptic ulcer disease is infection with Helicobacter pylori (H. pylori). These are microaerophilic, non-spore-forming, gram-negative, curved rod-shaped or coccoid bacteria. They play an important role in enhancing the aggressive properties of gastric contents and weakening of gastric and duodenal mucosal defense. The high frequency of chronic Helicobacter gastritis causes a high incidence of cancer. Therefore, the development of a model of Helicobacter-induced gastroduodenal diseases in vivo to search for alternative therapy for H. pylori infection is currently relevant.
Thus, the aim of the study was to develop a model of infectious (associated Helicobacter pylori) inflammation of the gastrointestinal tract. Assessment of the developed pathology was carried out by determining microscopic changes in the tissues of the gastrointestinal tract.
30 Mature male laboratory gerbils were used as a test system. Positive control animals were infected with a suspension of fresh H. pylori culture at a concentration of 2×109 CFU / ml in a volume of 0.5 ml with intragastric administration twice, once a day, for 2 days. Sterile trypton soy broth (a medium for H. pylori cultivation) was gavaged to negative control animals according to a similar scheme. The morphological analysis was based on the international classification of chronic gastritis (the Sydney system and its Houston modification).
As a result of the study, laboratory gerbils had a pathology of the gastric mucosa by the 24th week of the experiment.
After 8 weeks, the infected animals registered initial manifestations of catarrhal gastritis. By the end of the 16th week of the experiment, in addition to increasing gastritis, bacteria corresponding to H. pylori in their morphological forms were identified. By the end of the study, there was an inflammatory component in the gastric mucosa, atrophy of the glands, and erosive and ulcerative lesions of the mucous membrane. Bacterial forms corresponding to H. pylori was identified with a specific staining in the mucous membrane of the stomach. Pathological changes were observed mainly in the antral part of the stomach. The chosen system for assessing the severity of the pathology proved to be sufficient and objective, allowing us to fully analyze the development of pathology.
However, the use of this strain of H. pylori did not lead to the formation of ulcerative and metaplastic changes when observed at 24 weeks of pathology development, which was expected based on the literature data. Also, during this period of time, it was not possible to achieve the development of duodenite. It is likely that the used strain of bacteria did not have sufficient virulence, which should be taken into account in future studies.
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