title: No correlation of babA2 with vacA and cagA genotypes of Helicobacter pylori and grading of gastritis from peptic ulcer disease patients in Brazil.
abstract: BACKGROUND
  The babA2 gene, which encodes a blood-group antigen-binding adhesin that mediates attachment of Helicobacter pylori to human Lewis(b) antigens on gastric epithelial cells, has been associated with a higher risk of peptic ulcer and gastric cancer. The purpose of this study was to ascertain the frequency of babA2 genotype in H. pylori strains of patients with peptic ulcer and to correlate with other virulence factors.
  
  
  METHODS
  vacA, cagA, and babA2 genotypes of H. pylori were determined by using polymerase chain reaction (PCR). DNA was extracted from positive urease test gastric samples of 150 patients with peptic ulcer. Antrum and corpus biopsies were taken for histologic examination according to the updated Sydney system classification.
  
  
  RESULTS
  babA2 genotype was present in 104 (69.3%) and cagA in 113 (75.3%) gastric samples. No significant correlation was observed between babA2 and vacAs1 genotype or between babA2 and cagA status. The correlation of vacAs1 genotype with positive cagA was statistically significant ( p < .001). The babA2-positive strain was more frequently found from the gastric samples of men, than of women (p = .01). Strains harboring cagA, vacAs1, and babA2 genotypes had no association to the grading of gastritis, presence of glandular atrophy, or intestinal metaplasia. The simultaneous presence of cagA, vacAs1, and babA2 was found in 32.6% of the H. pylori strains.
  
  
  CONCLUSIONS
  babA2 genotype is frequently found in H. pylori strains from peptic ulcer disease in Brazil, although it has no significant correlation to the worsening of the gastritis and to other virulence markers such as vacAs1 and cagA.
authors.affiliation: Department of Gastroenterology, Serviço de Gastroenterologia, Hospital das Clinicas, University of Sao Paulo School of Medicine, Sao Paulo, Brazil. rmattar@hcnet.usp.br
authors.forename: Rejane
authors.initials: R
authors.lastname: Mattar
authors.forename: Anibal Ferreira
authors.initials: AF
authors.lastname: dos Santos
authors.forename: Jaime Natan
authors.initials: JN
authors.lastname: Eisig
authors.forename: Tomas Navarro
authors.initials: TN
authors.lastname: Rodrigues
authors.forename: Fernando Marcuz
authors.initials: FM
authors.lastname: Silva
authors.forename: Renato Micelli
authors.initials: RM
authors.lastname: Lupinacci
authors.forename: Kiyoshi
authors.initials: K
authors.lastname: Iriya
authors.forename: Flair José
authors.initials: FJ
authors.lastname: Carrilho
mesh_terms: D018829:Adhesins, Bacterial / Q000235:genetics / Q000378:metabolism; D000942:Antigens, Bacterial / Q000235:genetics / Q000378:metabolism; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism; D001483:Base Sequence; D005260:Female; D005756:Gastritis / Q000382:microbiology / Q000473:pathology*; D005838:Genotype; D016481:Helicobacter Infections / Q000382:microbiology / Q000473:pathology; D016480:Helicobacter pylori / Q000145:classification / Q000235:genetics / Q000378:metabolism / Q000472:pathogenicity*; D006801:Humans; D008297:Male; D008875:Middle Aged; D008969:Molecular Sequence Data; D010437:Peptic Ulcer / Q000382:microbiology / Q000473:pathology*; D012720:Severity of Illness Index; D014774:Virulence; D037521:Virulence Factors / Q000235:genetics* / Q000378:metabolism
chemical_list: D018829:Adhesins, Bacterial; D000942:Antigens, Bacterial; C400429:BabA protein, Helicobacter pylori; D001426:Bacterial Proteins; C074689:VacA protein, Helicobacter pylori; D037521:Virulence Factors; C080866:cagA protein, Helicobacter pylori