BabA-Leb binding intensity by radioimmunoassay with 125I-labelled conjugate showed a variation among individual H. pylori strains (18, 19). Marked heterogeneity in babA genetic content and BabA expression among H. pylori strains has been reported (19, 26). Regarding the relationship between the status of babA2 and BabA adhesion, 44% of babA2-negative strains were bound to Leb in Sweden, while 45% of babA2-positive strains showed no binding capacity to Leb in Portugal (23), possibly due to uncertain PCR detection with a single primer. We determined the status of babA2 by PCR with two primer pairs. babA2-positive or -negative
strains were each defined as being positive or negative by all primer
pairs. Where a contradiction was found, the PCR amplicons Selleck BMN 673 were subjected to sequence analysis to confirm the babA2 sequence. Evaluation for both BabA MBS and the subtle difference in the BabA amino acid sequence (middle region (AD1–5)) might allow determination of the extent of the BabA functional adhesion (18). Thus, the alignment of BabA sequences was analyzed in HPK5 and 20 randomly chosen isolates. The sequence analyses showed that the diversity of the BabA middle region was not a determinant of the degree of BabA-MBS, which is consistent with a previous report (24). Interestingly, find more the prevalence of AD2 (90.5%) was considerable greater than that reported previously (45.5%) (24), indicating that variation of the BabA middle region might exist within Japan. SabA is a prerequisite for the non-opsonic activation of human neutrophils (27), evokes a strong inflammatory response in human neutrophils (28) and has been identified as the sialic acid-dependent hemagglutinin based on sialidase-sensitive hemagglutination (29), suggesting that SabA is a candidate virulence molecule. However, the evidence explaining the association of SabA and its pathogenesis is not enough. SabA expression is regulated by CT-dinucleotide
repeats and the number of CT repeats depends on environmental conditions (5, AMP deaminase 17). Although the interaction between host sialyl-Lewis x and H. pylori SabA determines the degree of bacterial colonization in patients lacking gastric Leb, the sequence of the sabA gene, irrespective of CT repeats, is not a reliable predictor of SabA expression (30). Thus, the status of both babA2 and sabA genes does not always reflect these functions, implying that it is critical to evaluate the functional binding efficacy of BabA and SabA. The Leb-nonbinding strain with weak expression of BabA, but not the Leb-binding strain with strong expression of BabA, is associated with more severe mucosal injury and worse clinical outcome, suggesting that in vitro binding activity does not accurately reflect in vivo effects (19).