Published online Sep 28, 2014. doi: 10.3748/wjg.v20.i36.12767
Revised: April 8, 2014
Accepted: May 19, 2014
Published online: September 28, 2014
Processing time: 220 Days and 6.3 Hours
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.
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.