title: Polymorphisms of two fucosyltransferase genes (Lewis and Secretor genes) involving type I Lewis antigens are associated with the presence of anti-Helicobacter pylori IgG antibody.
abstract: Helicobacter pylori attach to the gastric mucosa with adhesin, which binds to Lewis b (Le(b)) or H type I carbohydrate structures. The Secretor (Se) gene and Lewis (Le) gene are involved in type I Le antigen synthesis. The present study was performed to investigate the possibility that Se and Le gene polymorphisms alter the risk of H. pylori infection. Two hundred thirty-nine participants were genotyped for Se and Le and tested for the presence of anti-H. pylori IgG antibodies. Using the normal gastric mucosa from 60 gastric cancer patients, we assessed immunohistochemically whether type I Le antigen expression depended on the Se and Le genotypes. The H. pylori infection rate was positively associated with the number of Se alleles (se/se group, 45.1%; Se/se group, 64.6%; and Se/Se group, 73.3%) and negatively associated with the number of Le alleles (le/le group, 76.4%; Le/le group, 68.3%; and Le/Le group, 55.6%). When the subjects were classified into three groups [low risk, (se/se, Le/Le) genotype; high risk, (Se/Se, le/le), (Se/Se, Le/le), and (Se/se, le/le) genotypes; moderate risk, other than low- or high-risk group], the odds ratio relative to the low-risk group was 3.30 (95% confidence interval, 1.40-7.78) for the moderate-risk group and 10.33 (95% confidence interval, 3.16-33.8) for the high-risk group. Immunohistochemical analysis supported the finding that Se and Le genotypes affected the expression of H. pylori adhesin ligands. We conclude that Se and Le genotypes affect susceptibility to H. pylori infection.
authors.affiliation: Division of Oncological Pathology, Aichi Cancer Center Research Institute, Nagoya 464-8681, Japan. yikehara@aichi.cc.pref.aichi.jp
authors.forename: Y
authors.initials: Y
authors.lastname: Ikehara
authors.forename: S
authors.initials: S
authors.lastname: Nishihara
authors.forename: H
authors.initials: H
authors.lastname: Yasutomi
authors.forename: T
authors.initials: T
authors.lastname: Kitamura
authors.forename: K
authors.initials: K
authors.lastname: Matsuo
authors.forename: N
authors.initials: N
authors.lastname: Shimizu
authors.forename: K
authors.initials: K
authors.lastname: Inada
authors.forename: Y
authors.initials: Y
authors.lastname: Kodera
authors.forename: Y
authors.initials: Y
authors.lastname: Yamamura
authors.forename: H
authors.initials: H
authors.lastname: Narimatsu
authors.forename: N
authors.initials: N
authors.lastname: Hamajima
authors.forename: M
authors.initials: M
authors.lastname: Tatematsu
mesh_terms: D000328:Adult; D000368:Aged; D000907:Antibodies, Bacterial / Q000097:blood; D044466:Asian People / Q000235:genetics; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005647:Fucosyltransferases / Q000235:genetics*; D005753:Gastric Mucosa / Q000382:microbiology; D005838:Genotype; D016481:Helicobacter Infections / Q000150:complications / Q000453:epidemiology / Q000276:immunology*; D016480:Helicobacter pylori / Q000276:immunology*; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood*; D007150:Immunohistochemistry; D007564:Japan / Q000453:epidemiology; D007983:Lewis Blood Group Antigens; D016256:Lewis X Antigen / Q000097:blood*; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D012150:Polymorphism, Restriction Fragment Length; D015995:Prevalence; D012307:Risk Factors; D013274:Stomach Neoplasms / Q000209:etiology / Q000235:genetics; D000097631:Galactoside 2-alpha-L-fucosyltransferase
chemical_list: D000907:Antibodies, Bacterial; D005647:Fucosyltransferases; D007074:Immunoglobulin G; D007983:Lewis Blood Group Antigens; D016256:Lewis X Antigen; D000097631:Galactoside 2-alpha-L-fucosyltransferase; C094162:Lewis Y antigen