title: Helicobacter pylori BabA expression, gastric mucosal injury, and clinical outcome.
abstract: OBJECTIVE
  The blood grou.
  
  
  METHODS
  We compared the ability of published PCR-based methods to assess BabA status with BabA immunoblotting and Lewis b (Le(b)) binding activity assays. We also used immunoblotting to examine the relationship between clinical presentation and levels of BabA expression.
  
  
  RESULTS
  Immunoblotting and Le(b) binding assays for 80 strains revealed 3 levels of BabA expression: BabA high producers (BabA-H) with Le(b) binding activity, BabA low producers (BabA-L) without Le(b) binding activity, and BabA-negative. BabA-negative strains lacked the babA gene. PCR methods to determine BabA status yielded poor results. babA1 sequences were never detected. BabA expression was examined in 250 strains from Western countries and 270 strains from East Asia. The results failed to confirm any relationship between triple-positive status (cagA-positive/vacA s1/BabA-H) and clinical outcome. BabA-negative strains typically were cagA-negative/vacA s2 and were associated with gastritis. BabA-L strains showed a higher level of mucosal injury and were associated more frequently with duodenal ulcer and gastric cancer than the other groups.
  
  
  CONCLUSIONS
  Information gained from currently used PCR-based methods must be interpreted with caution. Le(b) binding activity does not accurately reflect the severity of mucosal damage or the clinical outcome. Quantitation of BabA expression revealed that Le(b)-nonbinding BabA-L strains are associated with higher levels of mucosal injury and clinical outcome.
authors.affiliation: Department of Medicine, Michael E. DeBakey Veterans Affairs Medical Center and Baylor College of Medicine, Houston, Texas 77030, USA.
authors.forename: Saori
authors.initials: S
authors.lastname: Fujimoto
authors.forename: Olabisi
authors.initials: O
authors.lastname: Olaniyi Ojo
authors.forename: Anna
authors.initials: A
authors.lastname: Arnqvist
authors.forename: Jeng Yih
authors.initials: JY
authors.lastname: Wu
authors.forename: Stefan
authors.initials: S
authors.lastname: Odenbreit
authors.forename: Rainer
authors.initials: R
authors.lastname: Haas
authors.forename: David Y
authors.initials: DY
authors.lastname: Graham
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Yamaoka
mesh_terms: D000230:Adenocarcinoma / Q000235:genetics; D018829:Adhesins, Bacterial / Q000032:analysis / Q000235:genetics* / Q000378:metabolism; D017931:DNA Primers; D004381:Duodenal Ulcer / Q000235:genetics; D005753:Gastric Mucosa / Q000382:microbiology* / Q000473:pathology*; D005756:Gastritis / Q000235:genetics; D016480:Helicobacter pylori / Q000235:genetics* / Q000302:isolation & purification / Q000378:metabolism; D006801:Humans; D015151:Immunoblotting; D007983:Lewis Blood Group Antigens / Q000276:immunology; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000378:metabolism; D012720:Severity of Illness Index; D013274:Stomach Neoplasms / Q000235:genetics
chemical_list: D018829:Adhesins, Bacterial; C400429:BabA protein, Helicobacter pylori; D017931:DNA Primers; D007983:Lewis Blood Group Antigens; D012333:RNA, Messenger