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Background   Helicobacter pylori  can cause many kinds of gastric disorders, ranging from gastritis to gastric cancer. Cytotoxin-associated gene A (CagA) +  H. pylori  is more likely to cause gastric histopathologic damage than CagA –  H. pylori . However, the underlying mechanism needs to be further investigated.    Materials and methods  Mice were intragastrically administered equal amounts of CagA +  or CagA –  H. pylori . Four weeks later, 24 chemokines in stomachs were measured using a mouse chemokine array, and the phenotypes of the recruited gastric CD4 +  T cells were analyzed. The migration pathway was evaluated. Finally, the correlation between each pair among the recruited CD4 +  T cell sub-population,  H. pylori  colonization level, and histopathologic damage score were determined by Pearson correlation analysis.    Results  The concentration of chemokines, CCL3 and CX3CL1, were significantly elevated in CagA –  H. pylori -infected gastric mucosa than in CagA +  H. pylori -infected gastric mucosa. Among them, CX3CL1 secreted by gastric epithelial cells, which was elicited more effectively by CagA –  H. pylori  than by the CagA +  strain, dramatically promoted mucosal CD4 +  T cell migration. The expression of CX3CR1, the only known receptor of CX3CL1, was upregulated on the surface of gastric CD4 +  T cells in CagA –  H. pylori -infected stomach. In addition, most of the CX3CR1-positive gastric CD4 +  T cells were CD44 + CD69 – CCR7 –  effector memory T cells (Tem). Pearson correlation analysis showed that the recruited CX3CR1 + CD4 +  Tem cell population was negatively correlated with  H. pylori  colonization level and histopathologic damage score.    Conclusion  CagA –  H. pylori  promotes gastric mucosal CX3CR1 + CD4 +  Tem recruitment in mice.

Cytotoxin-Associated Gene A-Negative Helicobacter pylori Promotes Gastric Mucosal CX3CR1+CD4+ Effector Memory T Cell Recruitment in Mice