Table of Contents Author Guidelines Submit a Manuscript
Clinical and Developmental Immunology
Volume 2009, Article ID 850623, 10 pages
http://dx.doi.org/10.1155/2009/850623
Research Article

Immune Reactions Against Elongation Factor 2 Kinase: Specific Pathogenesis of Gastric Ulcer from Helicobacter pylori Infection

1Department of Bacteriology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Okayama 700-8558, Japan
2Graduate School of Health Science, Okayama University, 2-5-1 Shikata-cho, Okayama 700-8558, Japan
3Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Okayama 700-8558, Japan
4Department of Internal Medicine, Kagawa Prefectural Central Hospital, 5-4-16 Ban-cho, Takamatsu, Kagawa 760-8557, Japan

Received 3 December 2008; Accepted 13 February 2009

Academic Editor: Eiji Matsuura

Copyright © 2009 Kiyoshi Ayada et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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 ( ) but not in patients with chronic gastritis (CG; ) or in healthy volunteers (HC; ). 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.