Published online Sep 28, 2014. doi: 10.3748/wjg.v20.i36.12753
Revised: April 7, 2014
Accepted: May 19, 2014
Published online: September 28, 2014
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.
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.