Infection with Helicobacter pylori is associated with different human gastr
ic diseases. Biochemical studies, in vitro adherence assays, and in vivo an
imal models revealed that epithelial attachment of H. pylori can be mediate
d by the blood-group antigen-binding adhesin (BabA) targeting human Lewis(b
) surface epitopes, Studies with transgenic mice expressing the Lewis(b) ep
itope have shown that such attachment can alter disease outcome. In the cur
rent study, the presence of the babA2 gene encoding the adhesin was investi
gated in clinical isolates from a German population by using PCR and revers
e transcription-PCR. A positive genotype was correlated to allelic variatio
ns in the genes encoding VacA and CagA and also to the prevalence of duoden
al ulcer, distal gastric: adenocarcinoma, mucosa-associated lymphoid tissue
lymphoma, and antral gastritis. The presence of babA2 was significantly as
sociated with duodenal ulcer (P = 0.0002) and adenocarcinoma (P = 0.033). I
n contrast, type 1 strains (vacAs1- and cagA-positive) were associated with
only duodenal ulcer (P = 0.004) but not adenocarcinoma (P = 0.235). Genoty
pe presence of babA2, vacAs1, and cagA ("triple-positive" strains) showed a
highly significant correlation to the prevalence of ulcer (P = 0.000002) a
nd adenocarcinoma (P = 0.014) and discriminated significantly better betwee
n disease outcome than did the current type 1 classification. These results
indicate that the babA2 gene is of high clinical relevance and would he a
useful marker to identify patients who are at higher risk for specific H. p
ylori-related diseases.