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. 2023 Aug 14;29(30):4604–4615. doi: 10.3748/wjg.v29.i30.4604

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©The Author(s) 2023. Published by Baishideng Publishing Group Inc. All rights reserved.

This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/

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Hypothesis on correlation between concomitant infection with Helicobacter pylori and the presence of ulcerative colitis (inflammatory bowel disease), which has a pathological pattern of exacerbated T helper 2 response. The schematic shows HP-NAP being secreted into the gastric mucosa by Helicobacter pylori (H. pylori). Then, HP-NAP undergoes a process of transcytosis by endothelial cells, binding to the luminal side of the blood vessel. With this, there is an alteration in the expression of β-2-integrin, with the recruitment of neutrophils and monocytes, which carry out diapedesis. The recruited leukocytes secrete cytokines [interleukin (IL)-12 and IL-23], which promote a polarization of the circulating lymphocytes to a T helper 1 (Th1) pattern. The Th1 polarization causes a reduction in the Th2 response, this could explain the improvement of ulcerative colitis symptoms in patients infected with H. pylori. H. pylori: Helicobacter pylori; IL: Interleukin; Th: T helper; HP-NAP: Helicobacter pylori neutrophil-activating protein.