Abstract
Helicobacter pylori is one of the most common causes of chronic gastritis. With the development of the disease cellular inflammatory infiltrates composed of lymphocytes, plasma cells, and macrophages are formed in epithelium and lamina propria of the stomach. These cells are capable of secreting a number of active substances, including inducible nitric oxide synthase (iNOS). We examined the relationship between H. pylori and secretion of iNOS by cells of inflammatory infiltrates in chronic gastritis by light microscopy and immunohistochemistry. The data obtained indicate that stimulation of H. pylori immune system cells of the host organism during development of chronic gastritis causes increase in number of macrophages and lymphocytes in the inflammatory infiltrate of the gastric mucosa. This is accompanied with increased expression of inducible NO-synthase with excess free radicals in the tissues, which leads to secondary alterations and exacerbates the inflammation with impaired regeneration processes.
Highlights
Helicobacter pylori is one of the most common causes of chronic gastritis
H. pylori has been proved to be the etiological factor of type B chronic gastritis, gastric and duodenal ulcer, and other gastrointestinal diseases associated with the morphological changes of gastric mucosa and such dysregenerative manifestations as atrophy, metaplasia, and dysplasia underlying neoplastic processes [2]
It is known that inflammatory cellular infiltrate, containing mainly lymphocytes, plasmocytes, and macrophages, is generated in epithelium and lamina propria of the stomach during the development of chronic gastritis, including chronic H. pylori-associated gastritis [3]
Summary
Helicobacter pylori is one of the most common causes of chronic gastritis. Chronic H. pylori-associated gastritis develops in more than 50% of infected people [1]. H. pylori has been proved to be the etiological factor of type B chronic gastritis, gastric and duodenal ulcer, and other gastrointestinal diseases associated with the morphological changes of gastric mucosa and such dysregenerative manifestations as atrophy, metaplasia, and dysplasia underlying neoplastic processes [2]. It is known that inflammatory cellular infiltrate, containing mainly lymphocytes, plasmocytes, and macrophages, is generated in epithelium and lamina propria of the stomach during the development of chronic gastritis, including chronic H. pylori-associated gastritis [3]. Lymphocytes, plasmocytes, and macrophages cause the cytokine damage of gastric mucosa with the inducible NO-synthase (iNOS) being a mixed factor [4]
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