title: CagA and cytotoxicity of Helicobacter pylori are not markers of peptic ulcer in Japanese patients.
abstract: BACKGROUND
  The infection with cagA-positive Helicobacter pylori strains is reported to be associated with peptic ulcer disease in developed countries, but it is controversial in Asia. To investigate the relationship between the virulence factors of H. pylori and peptic ulcer disease in Japan, we compared these between ulcer and nonulcer patients.
  
  
  METHODS
  Seventy-four strains of clinically isolated H. pylori obtained from 22 gastric ulcer (GU), 23 duodenal ulcer (DU), and 29 chronic gastritis (CG) patients were studied. The presence of vacA and cagA gene was examined by polymerase chain reaction method using two different primer sets. We evaluated the proliferation-inhibiting and lethal cytotoxicity of culture supernatants using the alamarBlue assay.
  
  
  RESULTS
  The vacA gene was identified in all strains by the original primers. S1 strains were found in 90.9% (20/22) from GU, 95.7% (22/23) from DU, and 96.6% (28/29) from CG patients. The prevalence of cagA gene determined by the first, and second primers was 90.9% (20/22), 90.9% (20/22) in strains from GU, 87.0% (20/23), 91.3% (21/23) from DU, and 86.2% (25/29), 89.7% (26/29) from CG patients, respectively. The supernatant showed cytolethal effect in 95.5% (21/22) of strains from GU, in 100% (23/23) from DU, and in 93.1% (27/29) from CG patients. There was no significant difference in the prevalence of the virulence factors between H. pylori strains isolated from patients with peptic ulcers and those with chronic gastritis.
  
  
  CONCLUSIONS
  These results indicate that cagA gene status and the proliferation-inhibiting and lethal cytotoxicity of supernatant are not reliable markers of ulcerogenicity of H. pylori in Japanese patients.
authors.affiliation: Department of Gastroenterology, Jichi Medical School, Tochigi, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Tokumaru
authors.forename: K
authors.initials: K
authors.lastname: Kimura
authors.forename: K
authors.initials: K
authors.lastname: Saifuku
authors.forename: T
authors.initials: T
authors.lastname: Kojima
authors.forename: K
authors.initials: K
authors.lastname: Satoh
authors.forename: K
authors.initials: K
authors.lastname: Kihira
authors.forename: K
authors.initials: K
authors.lastname: Ido
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000942:Antigens, Bacterial; D001426:Bacterial Proteins / Q000235:genetics* / Q000494:pharmacology; D015415:Biomarkers / Q000032:analysis; D001706:Biopsy; D002455:Cell Division / Q000187:drug effects; D002648:Child; D002908:Chronic Disease; D003603:Cytotoxins / Q000235:genetics / Q000494:pharmacology; D004269:DNA, Bacterial / Q000235:genetics; D005260:Female; D005753:Gastric Mucosa / Q000382:microbiology / Q000473:pathology; D005756:Gastritis / Q000175:diagnosis / Q000382:microbiology; D005787:Gene Frequency; D016481:Helicobacter Infections / Q000150:complications / Q000175:diagnosis / Q000382:microbiology*; D016480:Helicobacter pylori / Q000145:classification / Q000235:genetics* / Q000472:pathogenicity*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010437:Peptic Ulcer / Q000175:diagnosis* / Q000382:microbiology*; D013045:Species Specificity
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D015415:Biomarkers; D003603:Cytotoxins; D004269:DNA, Bacterial; C074689:VacA protein, Helicobacter pylori; C080866:cagA protein, Helicobacter pylori