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Immune reactions against elongation factor 2 kinase: specific pathogenesis of gastric ulcer from Helicobacter pylori infection.

Ayada K, Yokota K, Kawahara Y, Yamamoto Y, Hirai K, Inaba T, Kita M, Okada H, Yamamoto K, Oguma K - Clin. Dev. Immunol. (2009)

Bottom Line: This antigen was over-expressed by a stressful (heat-stressed) environment, and was identified as elongation factor 2 kinase (EF-2K) by western blotting.The target cells (HGC-27) expressed EF-2K and MHC-class I together with costimulatory molecules from heat stress.This antigen specific immune mechanism could have a prominent role in the pathogenesis of GU.

View Article: PubMed Central - PubMed

Affiliation: Department of Bacteriology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan. k-ayada@sj8.so-net.ne.jp

ABSTRACT
Helicobacter pylori (H. pylori) infection is a definite causative factor for gastric ulcers (GUs). In the present study we detected a specific antigen of gastric epithelial cells (HGC-27) using cell ELISA, which was recognized by the sera of GU patients (n = 20) but not in patients with chronic gastritis (CG; n = 20) or in healthy volunteers (HC; n = 10). This antigen was over-expressed by a stressful (heat-stressed) environment, and was identified as elongation factor 2 kinase (EF-2K) by western blotting. The GU patients' lymphocytes stimulated by H. pylori specifically disrupted heat-stressed HGC-27 cells in a cytotoxic assay. In flow cytometry, the effector cells (lymphocytes) from GU patients were significantly differentiated to T helper type 1 lymphocyte (Th1) and cytotoxic T lymphocyte (CTL) as opposed to those from CG patients. The target cells (HGC-27) expressed EF-2K and MHC-class I together with costimulatory molecules from heat stress. This antigen specific immune mechanism could have a prominent role in the pathogenesis of GU.

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Flow cytometric analyses of target cells. (a) Typical analysis of EF-2K expression on HGC-27 cells is shown. The shadowed histogram indicates the EF-2K detected by GU sera in nontreated HGC-27 cells. And the bold histogram indicates the EF-2K detected by GU sera in heat-stressed HGC-27 cells. (b) Typical analysis of MHC class I molecule expression on HGC-27 cells is shown. The shadowed histogram indicates MHC class I molecules detected by PE-Cy5 conjugated mouse antihuman HLA-A, B, C antibody in nontreated HGC-27 cells and the bold histogram indicates MHC class I molecules detected by PE-Cy5 conjugated mouse antihuman HLA-A, B, C antibody in heat-stressed HGC-27 cells. The costimulatory molecules detected by FITC conjugated mouse antihuman CD80 antibody and PE conjugated mouse antihuman CD86 antibody on nontreated HGC-27 cells are shown in (c) and those of heat-stressed HGC-27 cells in (d). The heat stress enhanced the expression of EF-2K, MHC class I molecules, and costimulatory molecules on HGC-27 cells (target cells).
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fig5: Flow cytometric analyses of target cells. (a) Typical analysis of EF-2K expression on HGC-27 cells is shown. The shadowed histogram indicates the EF-2K detected by GU sera in nontreated HGC-27 cells. And the bold histogram indicates the EF-2K detected by GU sera in heat-stressed HGC-27 cells. (b) Typical analysis of MHC class I molecule expression on HGC-27 cells is shown. The shadowed histogram indicates MHC class I molecules detected by PE-Cy5 conjugated mouse antihuman HLA-A, B, C antibody in nontreated HGC-27 cells and the bold histogram indicates MHC class I molecules detected by PE-Cy5 conjugated mouse antihuman HLA-A, B, C antibody in heat-stressed HGC-27 cells. The costimulatory molecules detected by FITC conjugated mouse antihuman CD80 antibody and PE conjugated mouse antihuman CD86 antibody on nontreated HGC-27 cells are shown in (c) and those of heat-stressed HGC-27 cells in (d). The heat stress enhanced the expression of EF-2K, MHC class I molecules, and costimulatory molecules on HGC-27 cells (target cells).

Mentions: In the target cells, EF-2K was detected with GU patients' sera only in cases of heat stress treatment (Figure 5(a)). Further, the heat stress also enhanced the expression of MHC class I molecules and costimulatory molecules in target cells (Figures 5(b), 5(c), and 5(d)).


Immune reactions against elongation factor 2 kinase: specific pathogenesis of gastric ulcer from Helicobacter pylori infection.

Ayada K, Yokota K, Kawahara Y, Yamamoto Y, Hirai K, Inaba T, Kita M, Okada H, Yamamoto K, Oguma K - Clin. Dev. Immunol. (2009)

Flow cytometric analyses of target cells. (a) Typical analysis of EF-2K expression on HGC-27 cells is shown. The shadowed histogram indicates the EF-2K detected by GU sera in nontreated HGC-27 cells. And the bold histogram indicates the EF-2K detected by GU sera in heat-stressed HGC-27 cells. (b) Typical analysis of MHC class I molecule expression on HGC-27 cells is shown. The shadowed histogram indicates MHC class I molecules detected by PE-Cy5 conjugated mouse antihuman HLA-A, B, C antibody in nontreated HGC-27 cells and the bold histogram indicates MHC class I molecules detected by PE-Cy5 conjugated mouse antihuman HLA-A, B, C antibody in heat-stressed HGC-27 cells. The costimulatory molecules detected by FITC conjugated mouse antihuman CD80 antibody and PE conjugated mouse antihuman CD86 antibody on nontreated HGC-27 cells are shown in (c) and those of heat-stressed HGC-27 cells in (d). The heat stress enhanced the expression of EF-2K, MHC class I molecules, and costimulatory molecules on HGC-27 cells (target cells).
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC2712636&req=5

fig5: Flow cytometric analyses of target cells. (a) Typical analysis of EF-2K expression on HGC-27 cells is shown. The shadowed histogram indicates the EF-2K detected by GU sera in nontreated HGC-27 cells. And the bold histogram indicates the EF-2K detected by GU sera in heat-stressed HGC-27 cells. (b) Typical analysis of MHC class I molecule expression on HGC-27 cells is shown. The shadowed histogram indicates MHC class I molecules detected by PE-Cy5 conjugated mouse antihuman HLA-A, B, C antibody in nontreated HGC-27 cells and the bold histogram indicates MHC class I molecules detected by PE-Cy5 conjugated mouse antihuman HLA-A, B, C antibody in heat-stressed HGC-27 cells. The costimulatory molecules detected by FITC conjugated mouse antihuman CD80 antibody and PE conjugated mouse antihuman CD86 antibody on nontreated HGC-27 cells are shown in (c) and those of heat-stressed HGC-27 cells in (d). The heat stress enhanced the expression of EF-2K, MHC class I molecules, and costimulatory molecules on HGC-27 cells (target cells).
Mentions: In the target cells, EF-2K was detected with GU patients' sera only in cases of heat stress treatment (Figure 5(a)). Further, the heat stress also enhanced the expression of MHC class I molecules and costimulatory molecules in target cells (Figures 5(b), 5(c), and 5(d)).

Bottom Line: This antigen was over-expressed by a stressful (heat-stressed) environment, and was identified as elongation factor 2 kinase (EF-2K) by western blotting.The target cells (HGC-27) expressed EF-2K and MHC-class I together with costimulatory molecules from heat stress.This antigen specific immune mechanism could have a prominent role in the pathogenesis of GU.

View Article: PubMed Central - PubMed

Affiliation: Department of Bacteriology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan. k-ayada@sj8.so-net.ne.jp

ABSTRACT
Helicobacter pylori (H. pylori) infection is a definite causative factor for gastric ulcers (GUs). In the present study we detected a specific antigen of gastric epithelial cells (HGC-27) using cell ELISA, which was recognized by the sera of GU patients (n = 20) but not in patients with chronic gastritis (CG; n = 20) or in healthy volunteers (HC; n = 10). This antigen was over-expressed by a stressful (heat-stressed) environment, and was identified as elongation factor 2 kinase (EF-2K) by western blotting. The GU patients' lymphocytes stimulated by H. pylori specifically disrupted heat-stressed HGC-27 cells in a cytotoxic assay. In flow cytometry, the effector cells (lymphocytes) from GU patients were significantly differentiated to T helper type 1 lymphocyte (Th1) and cytotoxic T lymphocyte (CTL) as opposed to those from CG patients. The target cells (HGC-27) expressed EF-2K and MHC-class I together with costimulatory molecules from heat stress. This antigen specific immune mechanism could have a prominent role in the pathogenesis of GU.

Show MeSH
Related in: MedlinePlus