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World J Gastroenterol. Jun 14, 2017; 23(22): 3964-3977
Published online Jun 14, 2017. doi: 10.3748/wjg.v23.i22.3964
Molecular mimicry in Helicobacter pylori infections
Magdalena Chmiela, Weronika Gonciarz
Magdalena Chmiela, Weronika Gonciarz, Department of Immunology and Infectious Biology, Institute of Microbiology, Biotechnology and Immunology, Faculty of Biology and Environmental Protection, University of Lodz, 90-237 Lodz, Poland
Author contributions: Chmiela M designed and wrote the manuscript; Gonciarz W wrote some parts of the manuscript and designed the figure.
Supported by the National Science Center grants, No. UMO-2013/09/N/NZ6/00805 and No. UMO-2015/17/N/NZ6/03490.
Conflict-of-interest statement: No potential conflict of interest.
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: Magdalena Chmiela, MD, PhD, Professor, Department of Immunology and Infectious Biology, Institute of Microbiology, Biotechnology and Immunology, Faculty of Biology and Environmental Protection, University of Lodz, Banacha 12/16, 90-237 Lodz, Poland. chmiela@biol.uni.lodz.pl
Telephone: +48-42-6354186 Fax: +48-42-6655818
Received: January 18, 2017
Peer-review started: January 21, 2017
First decision: February 9, 2017
Revised: May 16, 2017
Accepted: June 1, 2017
Article in press: June 1, 2017
Published online: June 14, 2017
Processing time: 146 Days and 9.8 Hours
Abstract

Gram-negative bacteria Helicobacter pylori (H. pylori) colonize gastric mucosa in humans and increase the risk of serious diseases such as gastric and duodenal ulcers, stomach cancers and mucosa associated lymphoid tissue lymphoma. The role of H. pylori infection in the pathogenesis of several extragastric diseases has been suggested including immune thrombocytopenic purpura, iron deficiency anemia, vitamin D deficiency, cardiovascular diseases, diabetes mellitus and dermatological disorders. Also neurological diseases and even lung cancer have attracted researchers concern. The relation between H. pylori infection and a growth retardation in children has also been suggested. Many mechanisms of molecular mimicry between H. pylori and the host have been proposed as a pathogen strategy to manipulate the immune system of the host in order to remain unrecognized and avoid eradication. A lot of effort has been put into the demonstration of homologous sequences between H. pylori and host compounds. However, knowledge about how often autoantibodies or autoreactive T lymphocytes induced during H. pylori infections cause pathological disorders is insufficient. This review provides data on H. pylori antigenic mimicry and possible deleterious effects due to the induction of immune response to the components common to these bacteria and the host.

Keywords: Helicobacter pylori; Molecular mimicry; Anti-self response; Extragastric effects

Core tip: Molecular mimicry between Helicobacter pylori (H. pylori) and the host structures has been suggested as an effective mechanism of antibody production, potentially autoreactive. The chronic character of H. pylori infections increases the risk of such production and initiation or maintenance of H. pylori related pathological disorders triggered by the host effector immune mechanisms during infection. The panel of components common to H. pylori and the host is still increasing and thus the risk of autoimmune complications is an open problem.