Immune response to H. pylori

Abstract

The gastric mucosa separates the underlying tissue from the vast array of antigens that traffic through the stomach lumen. While the extreme pH of this environment is essential in aiding the activation of enzymes and food digestion, it also renders the gastric epithelium free from bacterial colonization, with the exception of one important human pathogen, H. pylori. This bacterium has developed mechanisms to survive the harsh environment of the stomach, actively move through the mucosal layer, attach to the epithelium, evade immune responses, and achieve persistent colonization. While a hallmark of this infection is a marked inflammatory response with the infiltration of various immune cells into the infected gastric mucosa, the host immune response is unable to clear the infection and may actually contribute to the associated pathogenesis. Here, we review the host responses involved during infection with H. pylori and how they are influenced by this bacterium.

Figure 1

Regulation of CD4⁺ T Cells During H pylori Infection. CD4⁺ T cell numbers increase in the gastric lamina propria of individuals infected with H pylori. These cells are predominantly Th1 cells characterized by their production of IFN-γ. Because the epithelium separates H pylori from CD4⁺ T cells, and also expresses key proteins associated with antigen presenting cells, the gastric epithelium, in addition to dendritic cells, could be involved in the presentation of antigens to these CD4⁺ T cells. The expression of inhibitory B7 related molecules along with CD4⁺ T cells with a regulatory T cell phenotype could be playing a role in limiting the function of effector CD4⁺ T cells.