OBJECTIVES: We tested whether the interaction between host gastric Le x antigen and the SabA protein of H. pylori determined gastric colonization density. METHODS: A total of 145 H. pylori-infected patients were assessed for their bacterial density and gastric Leb and sialyl-Lex 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. RESULTS: 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-Lex antigen (which interacts with SabA) (p < 0.001) only in those patients expressing weak or no gastric Leb antigen (which would interact with BabA), not in those with evident expression of gastric Leb antigen. CONCLUSIONS: In Taiwan, H. pylori isolates are 100% BabA-positive, but only 31% of them express SabA. The interaction between gastric sialyl-Lex and SabA of H. pylori determines the colonization density of patients expressing gastric Leb weakly or not at all.
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