Susceptibility to pediatric Helicobacter pylori infection correlates with the host responses of regulatory and effector T cells

Background: Tolerance to the early acquisition of Helicobacter pylori is suggested because of a biased ratio of regulatory to effector T cells in a mice model. This study investigated whether the CD4⁺CD25⁺ regulatory T (Treg) and CD4⁺CD25^- effector T (Teff) cell responses after H. pylori exposure determine H. pylori susceptibility in children. Methods: Treg and Teff cells from peripheral blood mononuclear cells (PBMCs) of H. pylori-infected and non-infected children were incubated with H. pylori protein. The cytokine levels and fraction of FOXP3⁺ to T cells were measured. FOXP3 expression was assessed by Western blotting and immunohistochemistry of gastric biopsies from dyspeptic children. Results: The fraction of FOXP3⁺ to CD4⁺CD25^high cells in PBMCs, FOXP3-positive staining and translation level in gastric tissues were higher in H. pyloriinfected children than in controls (P > 0.05). The translation levels of TGF-β1 in gastric tissues were higher in H. pylori-infected children than in controls (P > 0.05). After H. pylori challenge, H. pylori-infected children had a positive net-change in TGF-β1 from Treg cells, and a negative net-change of IFN-γ from Teff cells. Paradoxically, the non-infected controls had a negative net-change in TGF-β1 from Treg cells, and a positive net-change of IFN-γ from Teff cells. Conclusions: The host response of Treg cells with increases in FOXP3 and TGF-β1 combined with a reduction in IFN-γ by Teff cells may contribute to H. pylori susceptibility in children.