Diagnostic microbiology and infectious disease · 2025
Mechanism of Helicobacter pylori vacuolar cytotoxin a-induced gastric mucosal atrophy: A histopathological and immunohistochemical analysis.
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Wang Yang-Kun, Li Shen-Lin, Zhang Kai, Liu Yong-Jue, Li Ying-Ying, Zhang Fa-Shun, Niu Yao-Dong, Zhu Chao-Ya, Wang Su-Nan, Xu Si-Liang
Аннотация
OBJECTIVE: This study aims to examine the underlying mechanism of gastric mucosal atrophy induced by vacuolar cytotoxin A (VacA) produced by Helicobacter pylori.
METHODS: A total of 942 endoscopic biopsy and endoscopic submucosal dissection samples of gastric mucosa infected with H. pylori were subjected to detailed histomorphological and immunohistochemical analysis.
RESULTS: H. pylori exhibited specific adherence to surface mucus cells, proliferating extensively while producing and secreting VacA. The atrophic process was initiated by the upward migration and compensatory proliferation of cells in the deeper regions of the gastric pit, isthmus, and mucous neck cells. VacA disrupted the normal physiological organization and polarity of the proliferative zone, altering the proliferation patterns and directional growth of stem cells. This disruption resulted in a disordered state of cell proliferation. Insufficient downward migration of cells within the proliferative zone led to atrophy of the lamina propria glands in the gastric mucosa. This process was accompanied by epithelial cell proliferation and transformation, along with interstitial infiltration of lymphocytes, a small number of plasma cells, and neutrophils. These histopathological changes ultimately contributed to the characteristic atrophic gastritis associated with H. pylori infection.
CONCLUSION: A comprehensive understanding of the histopathological features of VacA-induced gastric mucosal atrophy is essential for the prevention and management of H. pylori-related gastric carcinogenesis.
METHODS: A total of 942 endoscopic biopsy and endoscopic submucosal dissection samples of gastric mucosa infected with H. pylori were subjected to detailed histomorphological and immunohistochemical analysis.
RESULTS: H. pylori exhibited specific adherence to surface mucus cells, proliferating extensively while producing and secreting VacA. The atrophic process was initiated by the upward migration and compensatory proliferation of cells in the deeper regions of the gastric pit, isthmus, and mucous neck cells. VacA disrupted the normal physiological organization and polarity of the proliferative zone, altering the proliferation patterns and directional growth of stem cells. This disruption resulted in a disordered state of cell proliferation. Insufficient downward migration of cells within the proliferative zone led to atrophy of the lamina propria glands in the gastric mucosa. This process was accompanied by epithelial cell proliferation and transformation, along with interstitial infiltration of lymphocytes, a small number of plasma cells, and neutrophils. These histopathological changes ultimately contributed to the characteristic atrophic gastritis associated with H. pylori infection.
CONCLUSION: A comprehensive understanding of the histopathological features of VacA-induced gastric mucosal atrophy is essential for the prevention and management of H. pylori-related gastric carcinogenesis.