title: Helicobacter pylori eradication decreases the expression of glycosylphosphatidylinositol-anchored complement regulators, decay-accelerating factor and homologous restriction factor 20, in human gastric epithelium.
abstract: BACKGROUND
  It has previously been reported that there is a strong correlation between the expression of glycosylphosphatidylinositol (GPI)-anchored complement membrane inhibitor in gastric epithelium and the severity of inflammation of gastric mucosa. To investigate the regulation of complement activity in gastric epithelium during Helicobacter pylori (H. pylori)-associated gastritis, the expression of GPI-anchored complement membrane inhibitors, decay-accelerating factor (DAF) and 20-kDa homologous restriction factor 20 (HRF20), and membrane cofactor protein (MCP), which is a transmembrane protein, were evaluated after removal of the H. pylori stimulus. Furthermore, the expression of the complement fragment, C3c, was also investigated.
  
  
  METHODS
  Forty-six patients with epigastric symptoms and endoscopically confirmed peptic ulcer or gastritis who had H. pylori infection of the gastric mucosa were enrolled in the present study. Biopsy specimens were obtained from the gastric antrum and corpus 1 month before and after eradication. Helicobacter pylori infection was determined by the rapid urease test, histology, and culture before eradication, and by histology, culture, and urea breath test after eradication. Gastric biopsy specimens obtained before and after eradication were evaluated for infiltration by neutrophils and mononuclear cells. The expression of complement membrane inhibitors, DAF, HRF20, and MCP and that of the main complement fragment, C3c, was immunohistochemically evaluated.
  
  
  RESULTS
  One month after the eradication of H. pylori, the infiltration by neutrophils and mononuclear cells in the gastric mucosa decreased significantly (P < 0.0001) as compared with that before eradication. The expression of DAF, HRF20, and C3c on gastric mucosal epithelium also significantly decreased in both the antrum and the corpus (P < 0.05) 1 month after eradication. However, no change was observed in the expression of MCP.
  
  
  CONCLUSIONS
  The decrease in the expression of GPI-anchored complement regulator and the complement after removal of a chronic microbial stimulus suggests that the gastric epithelium appears to undergo an aggressive stress of complement during H. pylori infection. Conclusively, DAF and HRF20 may play an important protective role against complement-mediated damage induced by chronic microbial stimuli in such a pathological condition.
authors.affiliation: Department of Internal Medicine and Bioregulation, Nagoya City University Graduate School of Medical Sciences, Japan.
authors.forename: Takashi
authors.initials: T
authors.lastname: Joh
authors.forename: Makoto
authors.initials: M
authors.lastname: Sasaki
authors.forename: Hiromi
authors.initials: H
authors.lastname: Kataoka
authors.forename: Satoshi
authors.initials: S
authors.lastname: Tanida
authors.forename: Keisuke
authors.initials: K
authors.lastname: Itoh
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Kondo
authors.forename: Naotaka
authors.initials: N
authors.lastname: Ogasawara
authors.forename: Tadayuki
authors.initials: T
authors.lastname: Oshima
authors.forename: Noriko
authors.initials: N
authors.lastname: Okada
authors.forename: Hirotaka
authors.initials: H
authors.lastname: Ohara
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Sano
authors.forename: Haruki
authors.initials: H
authors.lastname: Nakao
authors.forename: Satoshi
authors.initials: S
authors.lastname: Sobue
authors.forename: Makoto
authors.initials: M
authors.lastname: Itoh
mesh_terms: D000658:Amoxicillin / Q000627:therapeutic use; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D000897:Anti-Ulcer Agents / Q000627:therapeutic use; D018958:CD55 Antigens / Q000096:biosynthesis; D018957:CD59 Antigens / Q000096:biosynthesis; D017291:Clarithromycin / Q000627:therapeutic use; D015932:Complement C3c / Q000276:immunology; D003169:Complement Inactivator Proteins / Q000096:biosynthesis; D003165:Complement System Proteins / Q000276:immunology*; D005260:Female; D005753:Gastric Mucosa / Q000276:immunology* / Q000503:physiopathology; D005756:Gastritis / Q000188:drug therapy / Q000276:immunology; D017261:Glycosylphosphatidylinositols / Q000096:biosynthesis; D016481:Helicobacter Infections / Q000188:drug therapy / Q000276:immunology*; D016480:Helicobacter pylori; D006801:Humans; D008297:Male; D051916:Membrane Cofactor Protein / Q000096:biosynthesis; D008875:Middle Aged; D009853:Omeprazole / Q000627:therapeutic use; D010437:Peptic Ulcer / Q000188:drug therapy / Q000276:immunology; D011951:Receptors, Complement / Q000096:biosynthesis
chemical_list: D000900:Anti-Bacterial Agents; D000897:Anti-Ulcer Agents; D018958:CD55 Antigens; D018957:CD59 Antigens; D003169:Complement Inactivator Proteins; D017261:Glycosylphosphatidylinositols; D051916:Membrane Cofactor Protein; D011951:Receptors, Complement; D015932:Complement C3c; D000658:Amoxicillin; D003165:Complement System Proteins; D017291:Clarithromycin; D009853:Omeprazole