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World J Gastrointest Oncol. May 15, 2022; 14(5): 959-972
Published online May 15, 2022. doi: 10.4251/wjgo.v14.i5.959
Helicobacter pylori, gastric microbiota and gastric cancer relationship: Unrolling the tangle
Christos Liatsos, Apostolis Papaefthymiou, Nikolaos Kyriakos, Michail Galanopoulos, Michael Doulberis, Marios Giakoumis, Evangelia Petridou, Christos Mavrogiannis, Theodore Rokkas, Jannis Kountouras
Christos Liatsos, Apostolis Papaefthymiou, Nikolaos Kyriakos, Michail Galanopoulos, Marios Giakoumis, Department of Gastroenterology, 401 General Military Hospital of Athens, Athens 11525, Greece
Apostolis Papaefthymiou, Gastroenterology, University Hospital of Larissa, Larissa 41336, Greece
Michael Doulberis, Division of Gastroenterology and Hepatology, Medical University Department, Kantonsspital Aarau, Aarau 1234, Switzerland
Evangelia Petridou, Department of Microbiology, “Agia Sofia” Paediatric Hospital, Goudi, Athens 11527, Greece
Christos Mavrogiannis, Gastrointestinal and Liver Unit, Faculty of Nursing, Kifissia General and Oncology Hospital, Kaliftaki, N.Kifisia 14564, Greece
Theodore Rokkas, Gastroenterological Clinic, Henry Dunant Hospital, Athens 11525, Greece
Jannis Kountouras, Department of Internal Medicine, Second Medical Clinic, Ippokration Hospital, Aristotle University of Thessaloniki, Thessaloniki 41336, Macedonia, Greece
Author contributions: Liatsos C conceived the idea, provided revisions to the scientific manuscript content and participated in the writing, corrections and completion of all stages of the manuscript; Papaefthymiou A, Kyriakos N, Galanopoulos M, Doulberis M and Giakoumis M participated in manuscript writing and literature data finding; Petridou E contributed to literature data finding and editing; Mavrogiannis C, Rokkas T and Papaefthymiou A provided revisions and editing of the manuscript; Kountouras J participated in the writing, reviewing and final editing of the manuscript.
Conflict-of-interest statement: The authors declare having no conflict of interests for this article.
Open-Access: 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/
Corresponding author: Christos Liatsos, FEBG, MD, PhD, Director, Department of Gastroenterology, 401 General Military Hospital of Athens, Panagioti Kanellopoulou Ave, Athens 11525, Greece. cliatsos@yahoo.com
Received: March 19, 2021
Peer-review started: March 19, 2021
First decision: May 3, 2021
Revised: May 12, 2021
Accepted: April 9, 2022
Article in press: April 9, 2022
Published online: May 15, 2022
Processing time: 416 Days and 11.9 Hours
Abstract

Helicobacter pylori infection (Hp-I) represents a typical microbial agent intervening in the complex mechanisms of gastric homeostasis by disturbing the balance between the host gastric microbiota and mucosa-related factors, leading to inflammatory changes, dysbiosis and eventually gastric cancer. The normal gastric microbiota shows diversity, with Proteobacteria [Helicobacter pylori (H. pylori) belongs to this family], Firmicutes, Actinobacteria, Bacteroides and Fusobacteria being the most abundant phyla. Most studies indicate that H. pylori has inhibitory effects on the colonization of other bacteria, harboring a lower diversity of them in the stomach. When comparing the healthy with the diseased stomach, there is a change in the composition of the gastric microbiome with increasing abundance of H. pylori (where present) in the gastritis stage, while as the gastric carcinogenesis cascade progresses to gastric cancer, the oral and intestinal-type pathogenic microbial strains predominate. Hp-I creates a premalignant environment of atrophy and intestinal metaplasia and the subsequent alteration in gastric microbiota seems to play a crucial role in gastric tumorigenesis itself. Successful H. pylori eradication is suggested to restore gastric microbiota, at least in primary stages. It is more than clear that Hp-I, gastric microbiota and gastric cancer constitute a challenging tangle and the strong interaction between them makes it difficult to unroll. Future studies are considered of crucial importance to test the complex interaction on the modulation of the gastric microbiota by H. pylori as well as on the relationships between the gastric microbiota and gastric carcinogenesis.

Keywords: Helicobacter pylori infection; Gastric microbiota; Gastric cancer; Oncogenesis; Dysbiosis; Helicobacter pylori eradication

Core Tip: Gastric adenocarcinoma is a leading cause of cancer-related death in the world. Chronic gastric infection caused by Helicobacter pylori (H. pylori) is the strongest identified risk factor for gastric adenocarcinoma, prompting the World Health Organization to classify it as a class I carcinogen. It has been shown that in H. pylori-colonized patients, this pathogen accounts for more than 90% of all gastric microbiota modifying healthy microbiota and reducing its overall diversity. In this review, we tackle the complicated relationship between H. pylori, gastric microbiota and gastric cancer in an effort to unroll this tangle.