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. 2022 Sep 7;14(1):2120747. doi: 10.1080/19490976.2022.2120747

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© 2022 The Author(s). Published with license by Taylor & Francis Group, LLC.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 1. — Schematic representation of H. pylori pathogenesis and virulence factors. Upon entering the stomach, H. pylori begins to produce urease, which promotes the hydrolysis of urea to synthesize gastric acid. In this way, bacteria can resist gastric acidity and survive in the stomach. With the help of its helical shape and flagellum movement, H. pylori can easily penetrate the mucus layer and reach the gastric epithelium. After reaching the gastric epithelium, H. pylori colonizes gastric epithelial cells under the synergistic action of a variety of adhesins and outer membrane proteins (e.g., BabA, SabA, LabA, OipA, AlpA/AlpB, HopQ, and HopZ). Toxins (e.g., Cag A) are then injected into the host cells through the T4SS, leading to an inflammatory response. In addition, H. pylori can form biofilms composed of bacteria and a self-secreted extracellular matrix that adheres to inert and living surfaces; growth in biofilms facilitates the development of antibiotic resistance in H. pylori.