Topic Highlight
Copyright ©2014 Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Sep 28, 2014; 20(36): 12767-12780
Published online Sep 28, 2014. doi: 10.3748/wjg.v20.i36.12767
Effect of Helicobacter pylori on gastric epithelial cells
Shatha Alzahrani, Taslima T Lina, Jazmin Gonzalez, Irina V Pinchuk, Ellen J Beswick, Victor E Reyes
Shatha Alzahrani, Taslima T Lina, Irina V Pinchuk, Victor E Reyes, Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, United States
Jazmin Gonzalez, MSIII, School of Medicine, University of Texas Medical Branch, Galveston, TX 77555, United States
Irina V Pinchuk, Department of Internal Medicine, University of Texas Medical Branch, Galveston, TX 77555, United States
Ellen J Beswick, Departments of Molecular Genetics and Microbiology, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, United States
Victor E Reyes, Departments of Pediatricsand and Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, United States
Author contributions: All authors contributed to the writing of the different sections of this review; Alzahrani S took the leading role in organizing the topic and Reyes VE was responsible for the outline and editing.
Supported by National Institutes of Health, No. K22AI68712, No. R56DK090090-01; American Gastroenterological Association Research Scholar Award, NIH 1U54RR02614; The University of Texas Medical Branch Clinical and Translational Sciences Award; The American Cancer Society RSG-10-159-01-LIB, NIH 8UL1TR000041; The University of New Mexico Clinical and Translational Science Center; Alzahrani S founded by Saudi Arabia’s Ministry of Higher Education, the Saudi A Cultural Mission (SACM); Lina TT funded by Sealy Centre for Vaccine Development Pre-doctoral fellowship and McLaughlin Pre-doctoral Fellowship, UTMB
Correspondence to: Victor E Reyes, PhD, Departments of Pediatricsand and Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, United States. vreyes@utmb.edu
Telephone: +1-409-7723824 Fax: +1-409-7721761
Received: February 23, 2014
Revised: April 8, 2014
Accepted: May 19, 2014
Published online: September 28, 2014
Abstract

The gastrointestinal epithelium has cells with features that make them a powerful line of defense in innate mucosal immunity. Features that allow gastrointestinal epithelial cells to contribute in innate defense include cell barrier integrity, cell turnover, autophagy, and innate immune responses. Helicobacter pylori (H. pylori) is a spiral shape gram negative bacterium that selectively colonizes the gastric epithelium of more than half of the world’s population. The infection invariably becomes persistent due to highly specialized mechanisms that facilitate H. pylori’s avoidance of this initial line of host defense as well as adaptive immune mechanisms. The host response is thus unsuccessful in clearing the infection and as a result becomes established as a persistent infection promoting chronic inflammation. In some individuals the associated inflammation contributes to ulcerogenesis or neoplasia. H. pylori has an array of different strategies to interact intimately with epithelial cells and manipulate their cellular processes and functions. Among the multiple aspects that H. pylori affects in gastric epithelial cells are their distribution of epithelial junctions, DNA damage, apoptosis, proliferation, stimulation of cytokine production, and cell transformation. Some of these processes are initiated as a result of the activation of signaling mechanisms activated on binding of H. pylori to cell surface receptors or via soluble virulence factors that gain access to the epithelium. The multiple responses by the epithelium to the infection contribute to pathogenesis associated with H. pylori.

Keywords: Helicobacter pylori, Apoptosis, Gastric epithelial cells, Proinflammatory cytokines, Chronic inflammation, Gastric diseases, Gastric cancer

Core tip:Helicobacter pylori (H. pylori) is a gram negative bacterium that colonizes the gastric epithelium of more than half of the humankind. H. pylori use the gastric epithelial cells to manipulate the immune system to favor their survival and proliferation. In this review article, we focused on the mechanisms that facilitate the interaction between H. pylori and gastric epithelial cells, such as adhesion molecules, and we summarized the array of highly relevant outcomes of this interaction for the host.