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Background   Helicobacter pylori  causes acute and chronic gastric inflammation induced by proinflammatory cytokines and chemokines secreted by cells of the gastric mucosa, including gastric epithelial cells. Previous studies have demonstrated that the bacterial arginase, RocF, is involved in inhibiting T cell proliferation and CD3ζ expression, suggesting that arginase could be involved in a more general dampening of the immune response, perhaps by down-regulation of certain pro-inflammatory mediators.    Results  Global transcriptome analysis was performed on AGS gastric epithelial cells infected for 16 hours with a wild type  Helicobacter pylori  strain 26695, an arginase mutant ( rocF- ) or a  rocF   +   complemented strain.  H. pylori  infection triggered altered host gene expression in genes involved in cell movement, death/growth/proliferation, and cellular function and maintenance. While the wild type strain stimulates host inflammatory pathways, the  rocF-  mutant induced significantly more expression of  IL-8 . The results of the microarray were verified using real-time PCR, and the differential levels of protein expression were confirmed by ELISA and Bioplex analysis. MIP-1B was also significantly secreted by AGS cells after  H. pylori rocF-  mutant infection, as determined by Bioplex. Even though not explored in this manuscript, the impact that the results presented here may have on the development of gastritis, warrant further research to understand the underlying mechanisms of the relationship between  H. pylori  RocF and IL-8 induction.    Conclusions  We conclude that  H. pylori  arginase modulates multiple host signaling and metabolic pathways of infected gastric epithelial cells. Arginase may play a critical role in anti-inflammatory host responses that could contribute to the ability of  H. pylori  to establish chronic infections.

Transcriptional profiling of gastric epithelial cells infected with wild type or arginase-deficient Helicobacter pylori