Functional profile of gastric epithelial cells infected with Helicobacter pylori strains

• Helicobacter pylori infection causes imbalance between cell proliferation and cell apoptosis.
• H. pylori infection promotes the disintegration of proliferative gastric epithelial cells.
• Each H. pylori strain elicits differential responses in gastric epithelial cells.

Helicobacter pylori infection represents a key factor in the etiology of various gastro-duodenal diseases, ranging from chronic gastritis to the development of peptic ulcer disease and end-stage gastric cancer. In the present study, the 26695 and SS1 strains of H. pylori were used to study the differential functional profiles of gastric epithelial cells infected with H. pylori. The apoptosis rates in GES-1 cells were significantly increased 3, 12 and 24 h after H. pylori 26695 and SS1 infection. Moreover, apoptosis by cells infected with the H. pylori 26695 strain was significantly higher than cells infected with the SS1 strain of H. pylori. No significant changes in the proliferation rates of GES-1 cells were observed after H. pylori 26695 or SS1 infection at any time during the experimental period. Exposure to H. pylori 26695 and SS1 induced a significant decline in the adhesion rates of GES-1 cells in a time-dependent manner. Furthermore, H. pylori 26695 infection increased migration of GES-1 cells every hour during the whole experimental period compared with control cells. However, GES-1 cells infected with the H. pylori SS1 strain exhibited migration rates almost stable and comparable to those of control cells. These results indicate that the gastric epithelial cells respond differently depending on the H. pylori strains. This study indicates that the development of different gastric-related diseases may be a H. pylori strain-specific response.