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BMC Microbiol. 2012; 12: 175.
Published online Aug 13, 2012. doi:  10.1186/1471-2180-12-175
PMCID: PMC3438056
Transcriptional profiling of gastric epithelial cells infected with wild type or arginase-deficient Helicobacter pylori
Songhee H Kim,1 Rosa A Sierra,2 David J McGee,corresponding author1 and Jovanny Zabaletacorresponding author2
1Department of Microbiology and Immunology, Louisiana State University Health Sciences Center-Shreveport, 1501 Kings Highway, Shreveport, LA, 71130, USA
2Department of Pediatrics and Stanley S. Scott Cancer Center, Louisiana State University Health Sciences Center, New Orleans, LA, 70112, USA
corresponding authorCorresponding author.
Songhee H Kim: songhee75/at/hotmail.com; Rosa A Sierra: rsierr/at/lsuhsc.edu; David J McGee: dmcgee/at/lsuhsc.edu; Jovanny Zabaleta: jzabal/at/lsuhsc.edu
Received October 28, 2011; Accepted July 18, 2012.
Abstract
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.
Keywords: Arginase, Helicobacter pylori, Interleukin-8
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