Correlation of theHelicobacter pyloriadherence factor BabA with duodenal ulcer disease in four European countries

Abstract

Helicobacter pylori strains harboring the vacAs1, cagA and babA2 have been associated with ulcer disease (UD). We compared the prevalence of these different genotypes and adhesive properties in H. pylori infected patients with UD in four European countries. Genomic DNA was isolated from 314 H. pylori strains: Germany (GER; n=92), Sweden (SWE, n=74), Portugal (POR, n=91) and Finland (FIN, n=57). The frequencies of babA2 genotype varied from 35% to 60%. Triple-positive strains (vacAs1+, cagA+ and babA2+) were significantly associated with UD in GER and POR and were closely correlated with UD in FIN, but not in SWE. Classification as triple-positive strains had a higher specificity for detection of UD in GER, POR and FIN than type1 or cagA+ strains. In vitro adhesion assays revealed that Swedish strains showed high adhesion properties and were thus correlated with the diagnosis of UD, although PCR detected the babA2 gene at lower frequencies and failed to show a correlation with UD. This finding appears to reflect allelic variations of the babA2 gene in SWE, although adhesive properties of the strains are retained.

Correlation of Helicobacter pylori Genotypes with Gastric Histopathology in the Central Region of a South-European Country

“…babA2 were associated with peptic ulcer. The correlation of such clinical manifestation with these genotypes is consistent with earlier studies [35,41,52]. This is explained by the higher virulence and mucosal injury determined by such strains.…”

Prevalence of genotypes in Helicobacter pylori isolates from patients in eastern Turkey and the association of these genotypes with clinical outcome

“…Our results were similar to a previous study (1) (12,19,29) while it was 80-100% in Asian countries (16). We found a higher prevalence (62.1%) of babA2 than the result (53.8%) reported in a previous study (10) in Turkey.…”

Helicobacter pylori BabA Expression, Gastric Mucosal Injury, and Clinical Outcome

“…babA status (babA2 positive or negative) was determined by PCR using primer pairs and amplification conditions previously described (Figure 1). [5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22] Most of these primers were designed to detect the 10-bp signal sequence deletion of babA1, which is absent in babA2. Most previous studies used primer pair A (babA2S and babA2AS) ( Table 1) in which 2 nucleotides of the forward primer were changed from the known sequences of the babA2 gene from strain CCUG17875 (ie, AC to GT) ( Figure 1).…”

“…3 Most studies evaluating BabA status have used polymerase chain reaction (PCR) techniques based on detection of the 10-bp deletion to distinguish between the babA2 and babA1 genes ( Table 1). [5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22] However, the ability of such PCR-based strategies to detect the presence of a functional babA gene is questionable. For example, H pylori strains unable to bind to Lewis b antigen (Le b ) have been reported to contain signal peptide sequences that are identical to those of strains with a functional babA2 gene (eg, strain 26695).…”

“…24,25 Finally, not all of these PCR-based studies have shown an association between babA2 and intense cellular mucosal inflammations and/ or increased risk of peptic ulcer diseases and gastric cancer (Table 1). [10][11][12][13]19,20,22 Therefore, in the current study, we have compared results from PCR-based strategies that currently are used to predict BabA functional status with those from strategies that measure actual babA expression (ie, immunoblotting) and Le b binding.…”