Anti-Lewis X Antibody Promotes Helicobacter pylori Adhesion to Gastric Epithelial Cells

Abstract

ABSTRACT Lewis X (Le x ) antigen is expressed on the human gastric mucosa and the O-specific chain of lipopolysaccharides of Helicobacter pylori . This antigen can induce autoantibodies, which may be involved in bacterial colonization and thus deserve further investigation. Flow cytometry was used to examine the effects of anti-Le monoclonal antibodies (MAbs) on H. pylori adhesion. A babA2 mutant was also constructed to evaluate the effect of an anti-Le x MAb on adhesion. The bacterial agglutination and in situ adhesion assays were used to confirm the anti-Le x MAb effect on H. pylori adhesion. This study revealed that an anti-Le x MAb, but not an anti-Le b MAb or an anti-Le y MAb, could enhance the adhesion of H. pylori strains that expressed high levels of Le x antigen to AGS cells. The enhancement was not found on an H. pylori strain with a low level of Le x antigen. Anti-Le x MAb could increase the adhesion of both the wild-type strain and its isogenic babA2 mutant to AGS cells. When AGS cells were pretreated with anti-Le x MAb, the adhesion of the babA2 mutant also increased. Only anti-Le x MAb could promote bacterial agglutination, and the in situ adhesion assay further confirmed that adding anti-Le x MAb resulted in denser bacterial adhesion on the gastric epithelia collected from clinical patients. These results suggest anti-Le x MAb could specifically enhance the adhesion abilities of H. pylori strains through a mechanism by which anti-Le x MAb promotes bacterial aggregation and mediates bivalent interaction (antigen-antibody-antigen) between bacteria and host cells.