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ORIGINAL RESEARCH

How Does Helicobacter pylori Infection Cause Gastric Mucosal Atrophy

, , , , &
Pages 3619-3629 | Published online: 07 Jul 2022
 

Abstract

Objective

To investigate the occurrence and development of gastric mucosal atrophy due to Helicobacter pylori (Hp) infection and the accompanying histomorphological features.

Methods

Detailed histological observations and immunohistochemical examinations were conducted via 197 endoscopic biopsies and endoscopic submucosal dissection specimens of gastric mucosal atrophic lesions with gastric Hp infection. Detailed observation was made of columnar cells in the proliferative region of the deep gastric pit and the isthmus of the gastric gland, as well as the upper part of the glandular cervix.

Results

The infection of the gastric mucosa by Hp firstly led to the proliferative disorder of stem cells in the normal proliferative region of the gastric mucosa. This caused substantial propagation of cells in the proliferative region of the deep gastric pit and the isthmus of the gastric gland, as well as the upper part of the glandular cervix, as a means to replenish the damaged surface mucus cells. However, the propagation of stem cells in the proliferative region was insufficient for downward migration, and the normal physiological process of differentiation into fundic/pyloric gland cells was disrupted, resulting in glandular atrophy of the intrinsic layer of the gastric mucosa. Persistent Hp infection and disruption of stem cell proliferation in the proliferative region subsequently resulted in extensive segmental hyperplasia of the gastric mucosa and glandular atrophy of the lamina propria.

Conclusion

The occurrence, development, and histomorphological features of gastric mucosal atrophy due to gastric Hp infection provide a reliable pathological basis for precise treatment by clinicians and are of great significance for controlling the development of gastric cancer.

Abbreviations

HP, helicobacter pylori; GC, gastric cancer; ESD, endoscopic submucosal dissection; H&E, Hematoxylin and eosin; TBS, tris-buffered saline; DAB, diaminobenzidine; PBS, phosphate-buffered saline.

Ethical Statement

This study was conducted with approval from the Ethics Committee of Foresea Life Insurance Guangzhou General Hospital, Ethics Committee of Shenzhen Nanshan Hospital, Ethics Committee of No.989 Hospital of the PLA Joint Logistics Support Force, and Ethics Committee of the Third Affiliated Hospital of Zhengzhou University. This study was conducted in accordance with the declaration of Helsinki. Written informed consent was obtained from all participants.

Disclosure

The authors report no conflicts of interest in this work.

Additional information

Funding

Supported by the Key Scientific and Technological Research Project of Henan Province, No. 132102310008.