Interaction between host gastric Sialyl-Lewis X and H. pylori SabA enhances H. pylori density in patients lacking gastric Lewis B antigen.

We tested whether the interaction between host gastric Le(x) antigen and the SabA protein of H. pylori determined gastric colonization density. A total of 145 H. pylori-infected patients were assessed for their bacterial density and gastric Le(b) and sialyl-Le(x) expression. Their corresponding H. pylori isolates were tested for babA2 and sabA genotype by PCR. The sabA-genopositive PCR products were sequenced to check for mutations affecting SabA expression. The BabA and SabA expressions of each isolate were confirmed by Western blotting. All 145 H. pylori isolates were babA2-genopositive and expressed BabA. There were 116 (80%) sabA-genopositive isolates, but only 45 (31%) of the isolates expressed SabA. Sequence of sabA-genopositive PCR products was achieved in 92 isolates, of which 60% had regular CT repeat-pairs and the other 40% had a unique deletion of the CT repeats. Neither the deletion nor the different CT repeat-pairs in the sabA region were totally correlated with SabA expression, defined by Western blotting. H. pylori density was higher in those expressing gastric sialyl-Le(x) antigen (which interacts with SabA) (p < 0.001) only in those patients expressing weak or no gastric Le(b) antigen (which would interact with BabA), not in those with evident expression of gastric Le(b) antigen. In Taiwan, H. pylori isolates are 100% BabA-positive, but only 31% of them express SabA. The interaction between gastric sialyl-Le(x) and SabA of H. pylori determines the colonization density of patients expressing gastric Le(b) weakly or not at all.