Immune cell changes in Helicobacter pylori infection-induced glandular epithelial cell damage of the gastric mucosa.

Autor:	Wang SN; Shenzhen Polytechnic University, Shenzhen, China., Yun T; Department of Pathology, The 989th Hospital of the Joint Logistics Support Force of the Chinese People's Liberation Army, Luoyang, Henan, China., Zhu CY; Department of Pathology, Third Affiliated Hospital of Zhengzhou University, Shenzhen, China., Li P; Department of Pathology, Peking University Shenzhen Hospital, Shenzhen, China., Ge DF; Department of Pathology, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang, China., Li SL; Department of Pathology, The Fourth People's Hospital of Longgang District, Shenzhen, Shenzhen, China., Wang YK; Department of Pathology, The Fourth People's Hospital of Longgang District, Shenzhen, Shenzhen, China.
Jazyk:	angličtina
Zdroj:	Annals of medicine [Ann Med] 2024 Dec; Vol. 56 (1), pp. 2425072. Date of Electronic Publication: 2024 Nov 08.
DOI:	10.1080/07853890.2024.2425072
Abstrakt:	Objective: The purpose of this study was to investigate the relationship between Helicobacter pylori ( H. pylori ) infection-induced changes in gastric mucosal immune cells and glandular epithelial cell damage and the histopathological characteristics of these changes. Methods: We performed a detailed histomorphometry and immunohistochemical analysis of a total of 1635 H. pylori -infected gastric mucosal specimens. Results: Stage-wise features were as follows: Early stage of infection: H. pylori was colonized in the mucous layer, and very few neutrophils were visible in the layer. Gastric surface epithelial cell infection stage: H. pylori specifically and selectively adhered to the cytoplasm of the surface mucous cells, with the presence of a small number of neutrophils, eosinophils, and lymphocytes infiltration, which is termed early immune response. Compensatory mucous neck cell hyperplasia stage: proliferation of stem cells in the deep gastric pit and infiltration of a large number of lymphocytes in the superficial layer of lamina propria were observed, which is termed immune cell mobilization counterinsurgency. Lamina propria lesion stage: excessive upward migration of the proliferative area. Infiltration of a large number of lymphocytes, plasma cells, monocytes, macrophages, and other immune cells was observed in the whole layer of the gastric mucosa, which is termed automatic replication of immune cells. Abnormal proliferative transformation stage: presence of intranuclear milky globular body cells or signet-ring cell-like heterotypic cells at the junction of the gastric pit and the gastric gland, with proliferation of large numbers of immune cells and vacuolar degeneration of immune cells, which is termed the proliferation and degeneration of immune cells. Intraepithelial neoplasia stage: clonal hyperplasia of epithelial cells and immunosuppression. Conclusion: For controlling the occurrence and development of gastric cancer and effective immune intervention, it is essential to grasp the relationship between H. pylori infection-induced changes in gastric mucosal immune cells and glandular epithelial cell damage and its histopathological characteristics.
Databáze:	MEDLINE
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