title: The genetic diversity of Helicobacter pylori virulence genes is not associated with gastric atrophy progression.
abstract: Atrophy of the gastric mucosa is a precursor of intestinal-type gastric cancer, and Helicobacter pylori infection causes atrophic gastritis. The aim of this study was to determine whether the genetic diversity of H. pylori virulence genes is associated with the development and progression of gastric atrophy in humans. We isolated and cultured H. pylori strains from patients with gastric ulcer and duodenal ulcer accompanied by atrophic gastritis in background mucosa. H. pylori strains were stored at －80℃ prior to the experiments being carried out. We analyzed iceA, babA, vacA, cagA, and cagE genes by PCR. The cagA gene was analyzed through sequencing of the C-terminal region containing the EPIYA motif, which is related to tyrosine phosphorylation. Severe atrophy was observed in patients with gastric ulcer. The major phenotype of the vacA gene was s1c/m1 (93%). The cagA gene was detected in all strains. The cagE gene was not detected in 2 and 5 strains from the mild cases and severe cases, respectively. The major cagA EPIYA motif, which is amino acids repeat in the C terminus, was the A-B-D type (44 of 58 strains). The virulence genes were not statistically associated with the severity of atrophy in the background gastric mucosa in humans. Not only identification of bacterial virulence factors but also studies of the host response will be necessary to investigate the progression of gastric atrophy and subsequent cancer development in humans.
authors.affiliation: Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 700-8558, Japan.
authors.forename: Masahide
authors.initials: M
authors.lastname: Kita
authors.forename: Kenji
authors.initials: K
authors.lastname: Yokota
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Okada
authors.forename: Susumu
authors.initials: S
authors.lastname: Take
authors.forename: Ryuta
authors.initials: R
authors.lastname: Takenaka
authors.forename: Yoshiro
authors.initials: Y
authors.lastname: Kawahara
authors.forename: Keiji
authors.initials: K
authors.lastname: Oguma
authors.forename: Osamu
authors.initials: O
authors.lastname: Matsushita
authors.forename: Kazuhide
authors.initials: K
authors.lastname: Yamamoto
mesh_terms: D018829:Adhesins, Bacterial / Q000235:genetics; D000942:Antigens, Bacterial / Q000235:genetics; D001284:Atrophy; D001426:Bacterial Proteins / Q000235:genetics; D018450:Disease Progression; D004381:Duodenal Ulcer / Q000382:microbiology; D005260:Female; D005756:Gastritis / Q000382:microbiology*; D014644:Genetic Variation; D016481:Helicobacter Infections / Q000382:microbiology*; D016480:Helicobacter pylori / Q000235:genetics* / Q000472:pathogenicity; D006801:Humans; D008297:Male; D008875:Middle Aged; D013274:Stomach Neoplasms / Q000382:microbiology; D013276:Stomach Ulcer / Q000382:microbiology; D014774:Virulence; D037521:Virulence Factors / Q000235:genetics*
chemical_list: D018829:Adhesins, Bacterial; D000942:Antigens, Bacterial; C400429:BabA protein, Helicobacter pylori; D001426:Bacterial Proteins; C408644:IceA2 protein, Helicobacter pylori; C103937:PicB protein, Helicobacter pylori; C074689:VacA protein, Helicobacter pylori; D037521:Virulence Factors; C080866:cagA protein, Helicobacter pylori