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

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) g ene and Lewis (Le) gene are involved in type I Le antigen synthesis. The pr esent study was performed to investigate the possibility that Se and Le gen e polymorphisms alter the risk of H. pylori infection. Two hundred thirty-n ine participants were genotyped for Se and Le and tested for the presence o f anti-H. pylori IgG antibodies. Using the normal gastric mucosa from 60 ga stric cancer patients, we assessed immunohistochemically whether type I Le antigen expression depended on the Se and Le genotypes. The H. pylori infec tion rate was positively associated with the number of Se alleles (se/se gr oup, 45.1%; Se/se group, 64.6%; and Se/Se group, 73.3%) and negatively asso ciated 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 gr oups [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 h igh-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 highrisk group. Immunohistochemic al analysis supported the finding that Se and Le genotypes affected the exp ression of H. pylori adhesin ligands. We conclude that Se and Le genotypes affect susceptibility to H. pylori infection.