THE ROLE OF H. PYLORI INFECTION IN THE PATHOGENESIS OF INFLAMMATORY CHANGES IN THE GASTRIC MUCOSA


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Abstract

According to the World Health Organization, gastritis occurs in 60% of the population. The main cause of this disease is infection with the H.pylori bacterium, which is registered in 80-90% of cases. A number of other factors also affect gastritis, such as lifestyle, diet and predisposition to the development of this disease. In some people, the bacterium may not manifest itself for a long time, while in others it begins to multiply rapidly and destroy the gastric mucosa. It is worth highlighting that Helicobacter pylori is capable of causing not only chronic gastritis, but also pathologies such as peptic ulcer, adenocarcinoma, MALT lymphoma.
Goal. To evaluate the pathomorphological features of gastritis associated and not associated with H.pylori. In addition, take into account the role of tryptase TC in the formation of the inflammatory process.
Materials and methods. The analysis of biopsy materials, conclusions of pathologists in patients diagnosed with gastritis for the presence of Helicobacter pylori infection was carried out on the basis of the Voronezh Regional Pathology Bureau for the period 2017-2022. The morphological characteristics were evaluated using survey microscopy, an immunohistochemical method aimed at determining the presence of isolated tryptase and H. pylori and multiple immunofluorescence labeling, which allows identifying two antigens on one slice - tryptase TK and H. pylori.
Results. The OLGA international system (Operational Link on Gastritis Assessment) was used to assess inflammation in chronic gastritis, with the help of which the degree of inflammation and the stage of atrophy were determined.
Conclusion. The participation of H. pylori is often associated with the development of inflammation of the gastric mucosa, but in addition to this bacterium, immunocompetent cells also play a significant role.

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In Russia, over the past five years, the number of patients with gastritis has increased by 7%, which gives reason to consider this disease a serious health problem. The leading role in the occurrence of the disease is played by Helicobacter pylori (H. pylori), which is found, on average, in 80% of children and 90% of adults. Polish professor Valery Yavorsky in 1886 discovered a spiral bacterium while studying gastric lavages and was the first to suggest its significant role in the pathogenesis of stomach diseases. H. pylori, once in the gastric mucosa, produces a specific urease enzyme, with the help of which urea decomposes to ammonia and carbon dioxide. Ammonia provokes a change in the pH of the walls and causes an inflammatory process, which can subsequently lead to atrophy of the gastric mucosa. It is also very important to note that long-term persistent infection and inflammation of the gastric mucosa are favorable factors for the development of gastric cancer, which occupies the second place in the structure of oncological pathologies. P. Correa in 1988 described the successive stages in the development of gastric adenocarcinoma through the progression of precancerous changes in the gastric mucosa: chronic gastritis, chronic atrophic gastritis, intestinal metaplasia, dysplasia, gastric cancer [1]. The male population is more susceptible to the development of adenocarcinoma. Gender differences are associated with androgen receptors in stromal cells. It is important that for a long time the disease can be asymptomatic. As for the clinical picture, it manifests itself mainly when the immune system is weakened and severe stress occurs. In turn, the pathogenesis of H. pylori-associated gastritis also involves many immunocompetent cells, including mast cells (MCs), which, by regulating tryptase activity, induce changes in intercellular signaling, changes in the activity of other cells and non-cellular components, including including recruitment of granulocytes, increased capillary permeability, and ultimately inflammation [2-4]. In addition, mast cells can contribute to the development of intraorganic fibrosis and increase the activity of metalloproteinases, which can cause connective tissue remodeling. With regard to the treatment of chronic gastritis, the main goal is the eradication of the bacterium Helicobacter pylori. By preventing the attachment of bacteria, the necessary conditions for the healing of lesions will appear [5]. The appearance and development of gastritis not associated with H. pylori is also influenced by other factors, such as: autoimmune damage to the stomach, tobacco and alcohol abuse, unhealthy diet (fast food) and long-term medication (glucocorticosteroids and non-steroidal anti-inflammatory drugs (NSAIDs). NSAIDs can have a toxic, irritating effect on the gastric mucosa, causing damage and ulceration.Based on the foregoing, due to significant changes in lifestyle and nutrition, exposure to adverse environmental factors significantly reduces the number of patients with H. pylori infection [6]. Regarding the diagnosis of non-H. pylori gastritis, it is made in the absence of H. pylori in the stomach. Goal To study the morphological features of the inflammatory process in the gastric mucosa in patients with and without helicobacteriosis. Material and research methods Biopsy material, conclusions of pathologists in patients with gastritis according to the Voronezh Regional Pathological and Anatomical Bureau for the period 2017-2022. An analysis was made of the annual occurrence, belonging to age groups, staging categories of the inflammatory process, the presence of H. Pylori infection, localization of the malignant process, as well as the depth of the lesion. Morphological features were assessed using ready-made micropreparations stained with hematoxylin and eosin, alcian blue, and immunohistochemistry methods with antibodies to tryptase and H. pylori were also used to determine mast cells in inflammatory infiltrates. Results To assess inflammation in chronic gastritis, the OLGA morphological classification is used. A visual-analogue scale for the severity of infiltration of the epithelium and lamina propria of the gastric mucosa by mononuclear cells and neutrophilic leukocytes has been created. Mononuclear infiltration is defined as the severity of the process (normal, weak, moderate, severe), neutrophil infiltration is defined as the activity of the inflammatory process (normal, weak, moderate, severe). The degree of development of gastritis is assessed separately in the same biopsies according to the total intensity of lymphoplasmacytic and leukocytic infiltration in accordance with the visual analog scale and is also expressed in accordance with the table of its assessment in gradations from 0 to IV. Discussion The role of Helicobacter pylori infection has been repeatedly confirmed in the morphogenesis of inflammatory diseases of the gastric mucosa. However, the development of inflammatory responses is a multifactorial process that requires the involvement of cells of the immune system. The presence of infection of the gastric mucosa does not always correlate with the severity and activity of the inflammatory process. Conclusion The data obtained shed light on the morphogenetic role of H. pylori, however, the role of TK should be studied in more detail.

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About the authors

Victoria S. Aralova

Voronezh State Medical University named after N.N. Burdenko

Author for correspondence.
Email: vikaaralova2014@mail.ru
ORCID iD: 0000-0002-7290-9390
SPIN-code: 9051-2635
Russian Federation, 10 Studentskaya str., Voronezh, 394036, Russia

References

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