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. 2024 Jan 10;14:1330029. doi: 10.3389/fmicb.2023.1330029

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Copyright © 2024 Liu, Gao, Miao, Zhang, Zheng, Li, Zhou, Zhang, Li, Liu and Sun.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Process of Helicobacter pylori infection. (1) Helicobacter pylori enters the lumen of the host stomach. (2) Helicobacter pylori releases urease, decomposes the metabolites of other microorganisms (urea) into ammonia, changes the acidic environment of the stomach, which is conducive to the growth of H. pylori. (3) Helicobacter pylori releases adhesins (such as BabA, SabA, AlpA, HopQ, HopZ and OipA) that bind to specific receptors on gastric epithelial cells. (4) Helicobacter pylori releases CagA and VacA, which invade gastric epithelial cells and cause inflammatory reactions.