1. Introduction
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The major sites of Helicobacter pylori (H. pylori) infection are the stomach and duodenal bulbs, which are significantly associated with chronic gastritis, gastric mucosa atrophy and erosion, peptic ulcer, MALT lymphoma, and gastric cancer (Smith et al., 2017). In 1994, H. pylori were classified as a class I biological carcinogen by the World Health Organization (Ferreira et al., 2014). In 2015, the Kyoto Global Consensus Report on Helicobacter pylori identified H. pylori as an infectious disease (Sugano et al., 2015). In 2022, the United States Department of Health and Human Services listed H. pylori as a definite carcinogen. Helicobacter pylori are a highly heterogeneous bacterium, from which many virulence factors have been isolated and identified. Cytotoxin-associated gene A (CagA) and Vacuolating cytotoxin gene A (VacA) have been extensively studied as the virulence markers of H. pylori, since carrying these two genes has made H. pylori closely associated with the occurrence and development of many gastric diseases (Chey et al., 2017; Lee et al., 2021). Recent studies have shown that the CagA of H. pylori can cause genomic instability induced by BRCNESS. Moreover, H. pylori’s CagA can cause gastric cancer through a “hit and run” mechanism in the absence of p53 (Imai et al., 2021).
Clinically, based on the antibody expression of CagA and VacA, H. pylori can be classified into type I H. pylori infection (CagA+/VacA+) and type II H. pylori infection (CagA−/VagA−). Previous studies have found that type I H. pylori infection may contribute to the progression of gastric mucosal atrophy through its higher virulence factors and migration ability; however, there is no direct evidence to support this in the real gastric condition (Liu et al., 2021; Zhang et al., 2022). In this study, different types of H. pylori were analyzed to determine their infection characteristics using serology, pathology, and non-magnification white light endoscopy combined with Kimura-Takemoto classification, and the regular arrangement of collecting venules (RAC) as well. We have explored characteristics of different types of H. pylori causing gastric mucosa atrophy through virulence factors and migration ability in a specific population (50-60 years old), which may provide a new theoretical basis for clinical individual eradication therapy.
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