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

Lewis X (Lex) 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-Lex MAb on adhesion. The bacterial agglutination and in situ adhesion assays were used to confirm the anti-Lex MAb effect on H. pylori adhesion. This study revealed that an anti-Lex MAb, but not an anti-Leb MAb or an anti-Ley MAb, could enhance the adhesion of H. pylori strains that expressed high levels of Lex antigen to AGS cells. The enhancement was not found on an H. pylori strain with a low level of Lex antigen. Anti-Lex 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-Lex MAb, the adhesion of the babA2 mutant also increased. Only anti-Lex MAb could promote bacterial agglutination, and the in situ adhesion assay further confirmed that adding anti-Lex MAb resulted in denser bacterial adhesion on the gastric epithelia collected from clinical patients. These results suggest anti-Lex MAb could specifically enhance the adhesion abilities of H. pylori strains through a mechanism by which anti-Lex MAb promotes bacterial aggregation and mediates bivalent interaction (antigen-antibody-antigen) between bacteria and host cells.