title: Analysis of the expression of CagA and VacA and the vacuolating activity in 167 isolates from patients with either peptic ulcers or non-ulcer dyspepsia.
abstract: OBJECTIVE
  The goals of this study were: 1) to examine the prevalence of cytotoxin-associated protein (CagA), vacuolating cytotoxin (VacA), and the vacuolating cytotoxin activity (VCA) in vitro of infecting Helicobacter pylori isolates and 2) to clarify the relation between the expression of these virulence factors and the occurrence of peptic ulceration.
  
  
  METHODS
  One hundred sixty-seven clinical isolates of H. pylori from patients with peptic ulcer disease (gastric ulcer, 62 cases; duodenal ulcer, 48 cases) and nonulcer dyspepsia (57 cases) were studied regarding their genetic and phenotypic properties.
  
  
  RESULTS
  Type 1 bacteria, which had both CagA and VCA, and type 2 bacteria, which did not express either CagA or VCA, represented 62.9% and 7.8%, respectively; the remaining 29.4% had an intermediate phenotype, expressing either CagA independent of the presence of VCA (CagA+VCA-) or vice versa (CagA-VCA+). CagA+VCA- and CagA-VCA+ bacteria represented 17.4 % and 12.0%, respectively, both of which were more numerous than the type 2 category. The proportion of the CagA-positive isolates was significantly higher in both the duodenal ulcer (97.9%) and gastric ulcer (83.9%) patients than in the non-ulcer dyspepsia patients (61.4%) (p < 0.01). On the other hand, the proportion of VacA/VCA-positive isolates was not significantly different between peptic ulcer disease and non-ulcer dyspepsia.
  
  
  CONCLUSIONS
  The currently used classification of this bacterium based on the concomitant expression of CagA and VacA/VCA into the two major types is not adequate. The CagA-positive phenotype thus may be important as a virulence marker for peptic ulcer disease independent of the presence of VacA/VCA.
authors.affiliation: Department of Laboratory Medicine, Faculty of Medicine, Fukuoka University, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Takata
authors.forename: S
authors.initials: S
authors.lastname: Fujimoto
authors.forename: K
authors.initials: K
authors.lastname: Anzai
authors.forename: T
authors.initials: T
authors.lastname: Shirotani
authors.forename: M
authors.initials: M
authors.lastname: Okada
authors.forename: Y
authors.initials: Y
authors.lastname: Sawae
authors.forename: J
authors.initials: J
authors.lastname: Ono
mesh_terms: D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D001426:Bacterial Proteins / Q000633:toxicity*; D001431:Bacteriological Techniques; D015153:Blotting, Western; D003603:Cytotoxins / Q000633:toxicity*; D004381:Duodenal Ulcer / Q000209:etiology; D004415:Dyspepsia / Q000209:etiology*; D005260:Female; D005798:Genes, Bacterial / Q000235:genetics*; D006367:HeLa Cells; D016481:Helicobacter Infections / Q000150:complications / Q000382:microbiology*; D016480:Helicobacter pylori / Q000235:genetics* / Q000302:isolation & purification / Q000472:pathogenicity; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D010437:Peptic Ulcer / Q000209:etiology*; D010641:Phenotype; D016133:Polymerase Chain Reaction; D013270:Stomach / Q000382:microbiology; D013276:Stomach Ulcer / Q000209:etiology; D014617:Vacuoles; D014774:Virulence
chemical_list: D001426:Bacterial Proteins; D003603:Cytotoxins