ISOLATION OF A CELL-SURFACE COMPONENT OF HELICOBACTER-PYLORI THAT BINDS H-TYPE-2, LEWIS(A), AND LEWIS(B) ANTIGENS

Background & Aims: Individuals of blood group O and nonsecretors of AB O blood group antigens are more susceptible to peptic ulcers. The aim of this study was to determine if blood group antigens associated with group O or secretor status are epithelial cell receptors for Helicoba cter pylori. Methods: Bacterial binding and binding of monoclonal anti bodies to H type 2, Lewis(a), and Lewis(b) to Kato III, buccal epithel ial, and gastric mucosal cells were shown by flow cytometry. Bacterial outer membrane proteins eluted from H type 2, Lewis(a), or Lewis(b) w ere shown by polyacrylamide gel electrophoresis. Results: Kato III and human epithelial cells bound each monoclonal antibody; O cells bound move anti-H type 2 (P < 0.05). Binding indices for H. pylori correlate d with those for anti-H type 2 (P < 0.005) and anti-Lewis(b) (P < 0.00 1) but not anti-lewis(a). A 61-kilodalton protein was eluted from H ty pe 2, Lewis(a), or Lewis(b) Conclusions: Our results indicate that H t ype 2 is an important receptor for the 61-kilodalton bacterial adhesin , partly explaining increased susceptibility of individuals of blood g roup O to ulcers. Lewis(b) binds H. pylori move efficiently than Lewis (a). If these interactions occur in vivo, lack of Lewis(b) in mucosal fluids of nonsecretors may contribute to colonization by H. pylori.