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

Yao Jong Yang, Ching Chun Chuang, Hsiao Bai Yang, Cheng Chan Lu, Bor Shyang Sheu

研究成果: Article

3 引文 (Scopus)

摘要

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+CD25high 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.

原文English
頁(從 - 到)1277-1282
頁數6
期刊Pediatric Infectious Disease Journal
33
發行號12
DOIs
出版狀態Published - 2014 一月 1

指紋

Helicobacter Infections
Regulatory T-Lymphocytes
Helicobacter pylori
Eragrostis
Pediatrics
Stomach
Blood Cells
T-Lymphocytes
Western Blotting
Immunohistochemistry
Staining and Labeling
Cytokines
Biopsy

All Science Journal Classification (ASJC) codes

  • Pediatrics, Perinatology, and Child Health
  • Microbiology (medical)
  • Infectious Diseases

引用此文

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title = "Susceptibility to pediatric Helicobacter pylori infection correlates with the host responses of regulatory and effector T cells",
abstract = "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+CD25high 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.",
author = "Yang, {Yao Jong} and Chuang, {Ching Chun} and Yang, {Hsiao Bai} and Lu, {Cheng Chan} and Sheu, {Bor Shyang}",
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T1 - Susceptibility to pediatric Helicobacter pylori infection correlates with the host responses of regulatory and effector T cells

AU - Yang, Yao Jong

AU - Chuang, Ching Chun

AU - Yang, Hsiao Bai

AU - Lu, Cheng Chan

AU - Sheu, Bor Shyang

PY - 2014/1/1

Y1 - 2014/1/1

N2 - 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+CD25high 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.

AB - 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+CD25high 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.

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