title: Helicobacter pylori Lewis expression is related to the host Lewis phenotype.
abstract: OBJECTIVE
  Lewis antigens occur in human gastric epithelium and in Helicobacter pylori lipopolysaccharide; their expression is polymorphic in both. Autoimmune mechanisms induced by bacterial Lewis expression have been proposed to cause gastritis. The aim of this study was to examine the relationship between bacterial and host gastric Lewis expression, as determined by the erythrocyte Lewis(a/b) phenotype, and between gastric histopathology and bacterial Lewis expression.
  
  
  METHODS
  H. pylori Lewis expression was determined by enzyme immunoassays, erythrocyte Lewis phenotype was assessed by agglutination tests, and gastric histopathology was scored blindly.
  
  
  RESULTS
  The host Lewis phenotype was (a+b-) in 15, (a-b+) in 34, and (a-b-) in 17 patients, therefore expressing Lewis x, y, or neither as their major gastric epithelial Lewis type 2 antigen. H. pylori from patients with Lewis(a+b-) expressed Lewis x more than y (1147 +/- 143 vs. 467 +/- 128 optical density units [ODU]; P = 0.006), isolates from patients with Lewis(a-b+) expressed Lewis x less than y (359 +/- 81 vs. 838 +/- 96 ODU; P = 0.0001), and isolates from Lewis(a-b-) patients expressed Lewis x and y approximately equally. Gastritis was unrelated to H. pylori Lewis expression.
  
  
  CONCLUSIONS
  In mimicking host gastric epithelium, H. pylori cells not only express Lewis x and y, but the relative proportion of expression corresponds to the host Lewis phenotype, suggesting selection for host-adapted organisms.
authors.affiliation: Division of Infectious Diseases, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
authors.forename: H P
authors.initials: HP
authors.lastname: Wirth
authors.forename: M
authors.initials: M
authors.lastname: Yang
authors.forename: R M
authors.initials: RM
authors.lastname: Peek
authors.forename: K T
authors.initials: KT
authors.lastname: Tham
authors.forename: M J
authors.initials: MJ
authors.lastname: Blaser
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001706:Biopsy; D004912:Erythrocytes / Q000276:immunology*; D005260:Female; D005753:Gastric Mucosa / Q000382:microbiology / Q000473:pathology; D005756:Gastritis / Q000382:microbiology / Q000473:pathology; D005838:Genotype; D016481:Helicobacter Infections / Q000097:blood* / Q000175:diagnosis* / Q000276:immunology; D016480:Helicobacter pylori / Q000235:genetics* / Q000378:metabolism; D006801:Humans; D007249:Inflammation; D007983:Lewis Blood Group Antigens / Q000032:analysis / Q000096:biosynthesis / Q000235:genetics*; D016256:Lewis X Antigen / Q000032:analysis / Q000096:biosynthesis / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D011706:Pyloric Antrum
chemical_list: D007983:Lewis Blood Group Antigens; D016256:Lewis X Antigen; C094162:Lewis Y antigen