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World J Gastroenterol. Sep 28, 2014; 20(36): 12753-12766
Published online Sep 28, 2014. doi: 10.3748/wjg.v20.i36.12753
Immune evasion strategies used by Helicobacter pylori
Taslima T Lina, Shatha Alzahrani, Jazmin Gonzalez, Irina V Pinchuk, Ellen J Beswick, Victor E Reyes
Taslima T Lina, Shatha Alzahrani, Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, United States
Jazmin Gonzalez, MS-III 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 Pediatrics 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; Lina TT took the leading role in organizing the topic and Reyes VE was responsible for the outline and editing.
Supported by National Institutes of Health grants K22AI68712, 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; Taslima T Lina is funded by Sealy Centre for Vaccine Development Pre-doctoral fellowship and McLaughlin Pre-doctoral Fellowship, UTMB
Correspondence to: Victor E Reyes, PhD, Departments of Pediatrics and Microbiology and Immunology, University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555, United States. vreyes@utmb.edu
Telephone: +1-409-7723824 Fax: +1-409-7721761
Received: February 23, 2014
Revised: April 7, 2014
Accepted: May 19, 2014
Published online: September 28, 2014
Processing time: 220 Days and 6.4 Hours
Abstract

Helicobacter pylori (H. pylori) is perhaps the most ubiquitous and successful human pathogen, since it colonizes the stomach of more than half of humankind. Infection with this bacterium is commonly acquired during childhood. Once infected, people carry the bacteria for decades or even for life, if not treated. Persistent infection with this pathogen causes gastritis, peptic ulcer disease and is also strongly associated with the development of gastric cancer. Despite induction of innate and adaptive immune responses in the infected individual, the host is unable to clear the bacteria. One widely accepted hallmark of H. pylori is that it successfully and stealthily evades host defense mechanisms. Though the gastric mucosa is well protected against infection, H. pylori is able to reside under the mucus, attach to gastric epithelial cells and cause persistent infection by evading immune responses mediated by host. In this review, we discuss how H. pylori avoids innate and acquired immune response elements, uses gastric epithelial cells as mediators to manipulate host T cell responses and uses virulence factors to avoid adaptive immune responses by T cells to establish a persistent infection. We also discuss in this review how the genetic diversity of this pathogen helps for its survival.

Keywords: Helicobacter pylori; Immune response; Pattern recognition receptors; Phagocytes; T cells; Antigen presenting cells; Gastric epithelial cells; Vacuolating cytotoxin; T4SS

Core tip:Helicobacter pylori (H. pylori) is an important human pathogen that causes chronic infection in almost half of the population in the world. In the course of 30000 years of co-existence with humans, H. pylori has evolved extensive adaptations that allow it to successfully cause persistent infection in its host in the face of a vigorous innate and adaptive immune response. In this review, we discuss innate and adaptive immune responses to H. pylori and the mechanisms by which H. pylori evades immune-mediated clearance.