Helicobacter pylori virulence factors have been suggested to be important in determining the outcome of infection. The H. pylori adhesion protein BabA2 is thought to play a crucial role in bacterial colonization and in induction of severe gastric inflammation, particularly in combination with expression of CagA and VacA. However, the influence of these virulence factors on the pathogenesis of H. pylori infection is still poorly understood. To address this question, the inflammatory gene expression profiles for two groups of patients infected with triple-negative strains (lacking expression of cagA, babA2, and vacAs1 but expressing vacAs2) and triple-positive strains (expressing cagA, vacAs1, and babA2 but lacking expression of vacAs2) were investigated. The gene expression patterns in the antrum gastric mucosa from patients infected with different H. pylori strains were very similar, and no differentially expressed genes could be identified by pairwise comparisons. Our data thus suggest that there is a lack of correlation between the host inflammatory responses in the gastric mucosa and expression of the babA2, cagA, and vacAs1 genes.Helicobacter pylori infection is widespread in humans; it is present in 20 to 50% of the population in developed countries and 80% of the population in developing countries (43). Most infected individuals display only asymptomatic gastritis, whereas a small proportion develop severe disease, including peptic ulceration and gastric malignancy. Although the factors that determine the outcome of the infection are not well understood, bacterial virulence factors have been suggested to play important roles.One of the major virulence factors of H. pylori is the vacuolating cytotoxin (VacA), which causes cytoplasmic vacuolization in gastric epithelial cells (41). Another well-characterized virulence factor is the cytotoxin-associated antigen (CagA), which is encoded by one of the genes located in the cag pathogenicity island (PAI) (8). Strains expressing vacAs1 and/or cagA are present at a higher frequency in patients with duodenal ulcers, atrophic gastritis, and gastric carcinoma (2,5,13,17,23) and are referred to as type I strains. In contrast, type II strains, which lack the cagA gene, present a nontoxic form of VacA and are considered less virulent (37, 46). The blood group antigen binding adhesin (BabA), encoded by the babA2 gene, has previously been shown to mediate adherence of H. pylori to the Lewis b blood group antigen on human gastric epithelial cells (6,7,19). The attachment may facilitate H. pylori colonization and efficient delivery of virulence factors such as VacA or CagA to the host cells, resulting in severe gastric inflammation. It has indeed been shown that strains with babA2, particularly when it is present together with cagA and vacAs1 (referred to as triple-positive strains here), are more often associated with duodenal ulcers and adenocarcinoma than the strains without babA2 (15). Moreover, triplepositive strains are detected more frequently in patients with severe ...