Changes in Gastric Microbiota during Gastric Carcinogenesis
Korean J Helicobacter Up Gastrointest Res 2018;18(2):95-102
Published online June 10, 2018
© 2018 Korean College of Helicobacter and Upper Gastrointestinal Research.

Sun-Young Lee

Department of Internal Medicine, Konkuk University School of Medicine, Seoul, Korea
Correspondence to: Sun-Young Lee
Department of Internal Medicine, Konkuk University School of Medicine, 120-1 Neungdong-ro, Gwangjin-gu, Seoul 05030, Korea
Tel: +82-2-2030-7747, Fax: +82-2-2030-7748, E-mail: sunyoung@kuh.ac.kr
ORCID: https://orcid.org/0000-0003-4146-6686
Received January 6, 2018; Revised March 10, 2018; Accepted March 11, 2018.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
After World War II, the incidence of gastric cancer decreased rapidly in most of the developed countries; however, it remained high in countries where secondary prevention of gastric cancer is practiced without primary prevention (Helicobacter pylori eradication). In such countries, changes in gastric microbiota contribute to gastric carcinogenesis, and the composition of gastric microbiota is mainly determined by the status of H. pylori infection. In non-infected individuals with no history of H. pylori infection, gastric microbiota includes various bacteria, creating ideal microbial diversity. Because it is difficult for most bacteria to proliferate in an acidic environment in stomach, only few bacteria are present in non-infected individuals. Conversely, microbial dysbiosis with H. pylori predominance is often observed in infected individuals with unimpaired gastric secretory ability, because other bacteria cannot survive at low intragastric pH. Such microbial dysbiosis may rapidly lead to gastric carcinogenesis, resulting in diffuse-type gastric cancer. It is more frequent in young patients with unimpaired gastric secretory ability than in elderly patients with gastric atrophy and metaplasia. Lastly, bacteria producing carcinogenic N-nitrosamine compounds are often detected in individuals with past or chronic H. pylori infection, because of the loss of gastric secretory ability. Such an unideal microbial diversity observed at high intragastric pH may slowly lead to gastric carcinogenesis, in turn resulting in gastric adenoma or intestinal-type gastric cancer. To prevent gastric carcinogenesis, changes in the composition of gastric microbiota should be studied in conjunction with intragastric acidity, which depends on the status of H. pylori infection.
Keywords : Carcinogenesis; Helicobacter pylori; Microbiota; Stomach


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