title: Mucosal production of antigastric autoantibodies in Helicobacter pylori gastritis.
abstract: BACKGROUND
  Apart form bacterial virulence factors of Helicobacter pylori, certain host factors influence the pathogenesis of H. pylori gastritis. In particular, antigastric autoantibodies that are detectable in the sera of a substantial proportion of H. pylori were shown to correlate with the development of gastric atrophy. The aim of this study was to analyze the possible antigastric autoimmune response in H. pylori gastritis at the site where the action is, i.e. , in the gastric mucosa.
  
  
  METHODS
  Gastric biopsy specimens from antrum and corpus mucosa of 24 H. pylori-infected and of 33 noninfected patients were cultured for 3 days, and tissue culture supernatants were analyzed for the amount of locally produced IgA and IgG. Antigastric autoantibodies were screened in the sera and in the supernatants by means of immunohistochemistry.
  
  
  RESULTS
  The infected patients had significantly higher concentrations of locally produced IgA, whereas the IgG concentrations were virtually the same in infected and noninfected patients. IgG or IgA antigastric autoantibodies, or both, were detectable only in the sera (38%) and supernatants (17%) of infected patients. Interestingly, the patient with the strongest local autoimmune response showed body-predominant H. pylori gastritis, with destruction of gastric glands and atrophy of the body mucosa.
  
  
  CONCLUSIONS
  These results demonstrate that antigastric autoimmune reactions are detectable at the site of the disease and might be relevant for the pathogenesis of gastric mucosa atrophy in H. pylori gastritis.
authors.affiliation: Institute of Pathology and Department of Internal Medicine I, University of Erlangen-Nuremberg, Germany.
authors.forename: G
authors.initials: G
authors.lastname: Faller
authors.forename: S
authors.initials: S
authors.lastname: Ruff
authors.forename: N
authors.initials: N
authors.lastname: Reiche
authors.forename: J
authors.initials: J
authors.lastname: Hochberger
authors.forename: E G
authors.initials: EG
authors.lastname: Hahn
authors.forename: T
authors.initials: T
authors.lastname: Kirchner
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001323:Autoantibodies / Q000378:metabolism*; D005260:Female; D005753:Gastric Mucosa / Q000276:immunology*; D005756:Gastritis / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D016481:Helicobacter Infections / Q000276:immunology* / Q000473:pathology; D016480:Helicobacter pylori; D006801:Humans; D007106:Immune Sera; D007070:Immunoglobulin A / Q000378:metabolism; D007074:Immunoglobulin G / Q000378:metabolism; D008297:Male; D008875:Middle Aged
chemical_list: D001323:Autoantibodies; D007106:Immune Sera; D007070:Immunoglobulin A; D007074:Immunoglobulin G