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 CD4CD25 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. pylori-infected 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.
From the *Departments of Pediatrics; †Internal Medicine; ‡Pathology; and §Institute of Clinical Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan; and ¶Department of Pathology, Ton-Yen General Hospital, Hsinchu County, Taiwan.
Yao-Jong
YJ
Yang
Ching-Chun
CC
Chuang
Hsiao-Bai
HB
Yang
Cheng-Chan
CC
Lu
Bor-Shyang
BS
Sheu
D001706:Biopsy; D015153:Blotting, Western; D015496:CD4-Positive T-Lymphocytes / Q000737:chemistry / Q000276:immunology*; D002478:Cells, Cultured; D002648:Child; D002675:Child, Preschool; D004198:Disease Susceptibility; D005260:Female; D051858:Forkhead Transcription Factors / Q000032:analysis; D005753:Gastric Mucosa / Q000473:pathology; D016481:Helicobacter Infections / Q000276:immunology*; D016480:Helicobacter pylori / Q000276:immunology*; D006801:Humans; D007150:Immunohistochemistry; D007371:Interferon-gamma / Q000378:metabolism; D053645:Interleukin-2 Receptor alpha Subunit / Q000032:analysis; D007963:Leukocytes, Mononuclear / Q000276:immunology; D008297:Male; D016176:T-Lymphocyte Subsets / Q000737:chemistry / Q000276:immunology*; D053773:Transforming Growth Factor beta1 / Q000032:analysis
C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; C508017:IL2RA protein, human; D053645:Interleukin-2 Receptor alpha Subunit; D053773:Transforming Growth Factor beta1; D007371:Interferon-gamma