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Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Oct 28, 2015; 21(40): 11450-11457
Published online Oct 28, 2015. doi: 10.3748/wjg.v21.i40.11450
Dysbiotic infection in the stomach
Hisashi Iizasa, Shyunji Ishihara, Timmy Richardo, Yuichi Kanehiro, Hironori Yoshiyama
Hisashi Iizasa, Timmy Richardo, Yuichi Kanehiro, Hironori Yoshiyama, Department of Microbiology, Shimane University Faculty of Medicine, Shimane 693-8501, Japan
Shyunji Ishihara, Department of Internal Medicine II, Shimane University Faculty of Medicine, Shimane 693-8501, Japan
Author contributions: Yoshiyama H contributed to the study idea, study design, literature search, manuscript writing and final revision of the article; Iizasa H, Ishihara S, Richardo T and Kanehiro Y contributed to the manuscript writing and the final revision of the article.
Supported by (in part) Grant-in-Aid for Scientific Research from the Ministry of Education; Culture, Science and Technology of Japan, No. 26460546 (to Yoshiyama H).
Conflict-of-interest statement: The authors have no conflict of interest to report.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (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: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Hironori Yoshiyama, MD, PhD, Department of Microbiology, Shimane University Faculty of Medicine, 89-1 Enya, Izumo, Shimane 693-8501, Japan. yosiyama@med.shimane-u.ac.jp
Telephone: +81-853-202146 Fax: +81-853-202147
Received: May 18, 2015
Peer-review started: May 20, 2015
First decision: June 23, 2015
Revised: July 10, 2015
Accepted: September 14, 2015
Article in press: September 15, 2015
Published online: October 28, 2015
Processing time: 158 Days and 0.4 Hours
Abstract

Microbiota in human alimentary tract plays important roles for homeostatic maintenance of the body. Compositional difference of gut microbiota is tightly associated with susceptibility of many diseases, including inflammatory diseases, obesity, diabetes mellitus, cancer, and atherosclerosis. “Dysbiosis” refers to a state of imbalance among the colonies of microorganisms within the body, which brings abnormal increase of specific minor components and decrease in the normally dominant species. Since stomach secrets strong acid for its digestive role, this organ has long been thought a sterile organ. However, the discovery of Helicobacter pylori (H. pylori) has changed the concept. This bacterium has proven to cause gastritis, peptic ulcer, and gastric cancer. However, recent cross-sectional studies revealed that H. pylori carriers had a decreased risk of developing immunological diseases, such as asthma. H. pylori coinfection also suppresses inflammatory bowel diseases. This review describes human gastric microbiota by discussing its mutual interaction and pathogenic enrollment. Gastric “dysbiosis” may affect host inflammatory response and play important role for gastric pathogenesis. We will topically discuss enrollment of dysbiosis for genesis of gastric cancer as well as for disruption of immunological homeostasis affecting oncogenic resistance.

Keywords: Stomach; Microbiota; Dysbiosis; Helicobacter pylori; Epstein-Barr virus

Core tip: The imbalance of microflora in the gut induces dysbiosis. Altered gut microflora is known to be associated with inflammatory diseases, obesity, diabetes, cancer, and atherosclerosis. Little is known about gastric microflora, which will also interacts with bacteria, viruses and funguses. In this review, we discuss that dysbiosis in the stomach may disrupt immunological homeostasis, reduce of carcinogenic resistance, and induce gastric cancer.