title: Th response to Helicobacter pylori differs between patients with gastric ulcer and duodenal ulcer.
abstract: OBJECTIVE
  Helicobacter pylori (H. pylori) infection induces both gastric (GU) and duodenal ulcers (DU). We examined whether host immunological response to H. pylori determines different disease outcomes.
  
  
  METHODS
  Thirty-two GU and 28 DU patients infected with H. pylori, and 24 dyspeptic patients without infection were enrolled. The constituents of cellular infiltrates in biopsies from each patient were determined and lymphokines secreted by stimulated T cells were measured. Serum concentrations of IgG subclasses specific to H. pylori were measured.
  
  
  RESULTS
  Low pepsinogen I and high pepsinogen II levels were observed in GU patients, while a high pepsinogen I level was found in DU patients. T cells predominate over other cell types in both GU and DU patients. GU patients had a higher number of T cells (p < 0.01) and lower plasma cells (p < 0.05) than those in DU patients. T cells from GU patients produced greater amounts of IFN-gamma and less IL-4 than those in DU patients (p < 0.01). GU patients had a higher serum level of IgG2 specific to H. pylori than that in DU patients (p < 0.01).
  
  
  CONCLUSIONS
  Th response by gastric T cells in GU patient was more polarized to Th1 as compared with that in DU patients, suggesting that a distinct immune response to H. pylori induces different disease outcomes.
authors.affiliation: Department of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Itoh
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Seno
authors.forename: Toru
authors.initials: T
authors.lastname: Kita
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Chiba
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Wakatsuki
mesh_terms: D000328:Adult; D015331:Cohort Studies; D016207:Cytokines / Q000032:analysis / Q000378:metabolism*; D018450:Disease Progression; D004381:Duodenal Ulcer / Q000382:microbiology* / Q000473:pathology; D005260:Female; D005434:Flow Cytometry; D005500:Follow-Up Studies; D005753:Gastric Mucosa / Q000276:immunology / Q000473:pathology; D005755:Gastrins / Q000032:analysis / Q000378:metabolism; D016481:Helicobacter Infections / Q000175:diagnosis / Q000276:immunology*; D016480:Helicobacter pylori / Q000276:immunology* / Q000302:isolation & purification; D006801:Humans; D007074:Immunoglobulin G / Q000032:analysis; D007413:Intestinal Mucosa / Q000276:immunology / Q000473:pathology; D008297:Male; D008875:Middle Aged; D020116:Pepsinogen A / Q000032:analysis / Q000378:metabolism; D018570:Risk Assessment; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D013276:Stomach Ulcer / Q000382:microbiology* / Q000473:pathology; D016176:T-Lymphocyte Subsets / Q000276:immunology
chemical_list: D016207:Cytokines; D005755:Gastrins; D007074:Immunoglobulin G; D020116:Pepsinogen A