The team evaluated the relationship between Helicobacter pylori blood group antigen binding adhesin (BabA) status with gastric epithelial cell turnover and premalignant gastric lesions.
The findings of the study were reported in the October issue of Gut.
H. pylori babA2 mediates bacterial adherence to human blood group antigens on gastric epithelium.
Strains harboring babA2 were recently found to be associated with peptic ulcer and gastric cancer.
However, the role of babA2 in cellular turnover, severity of gastritis, and premalignant changes is poorly understood.
Therefore the authors correlated H. pylori babA2, vacuolating toxin (vacA), and cytotoxin associated gene A (cagA) genotypes with the severity of gastric inflammation and epithelial cell turnover.
The H. pylori isolates were obtained from a group of 104 Chinese patients from an area with a high incidence of gastric cancer.
Genotype variants of babA2, vacA, and cagA were determined by polymerase chain reaction.
|babA2+ strains linked with:|
- Higher lymphocytic infiltration
- Glandular atrophy
- Intestinal metaplasia in antrum
Antrum and corpus histopathology was examined according to the updated Sydney classification.
Of the included patients, 98% harbored cagA+ strains and all had vacA s1 genotype.
The babA2+ strains were found in 80% of patients.
They were found to be associated with higher lymphocytic infiltration, presence of glandular atrophy (odds ratio (OR) 7.5), and intestinal metaplasia (OR 7.4) in the antrum.
Increased epithelial proliferation was also noted in individuals infected with babA2+ strains.
Nonetheless, strains harboring cagA+/vacA s1 genotypes lacked this association in the absence of babA2.
Author J. Yu, of the Prince of Wales Hospital, Chinese University of Hong Kong, concluded on behalf of the group, "The presence of babA2+ H. pylori strains alone or in combination with cagA+ and vacA s1 was associated with the presence of preneoplastic gastric lesions."