DNA-DNA hybridization demonstrates apparent genetic differences between Helicobacter pylori from patients with duodenal ulcer and asymptomatic gastritis.

We asked whether different clinical outcomes of Helicobacter pylori infection might be a reflection of genetic differences in infecting organisms. Using DNA-DNA hybridization we examined whether hybridization levels grouped H. pylori isolates corresponding to the type of disease (gastric ulcer, duodenal ulcer, asymptomatic gastritis) from which they were recovered. Target DNAs were prepared from H. pylori strains cultured from gastric biopsy specimens of 25 patients; 5 with gastric ulcers, 9 with duodenal ulcers, and 11 from asymptomatic volunteers endoscopically proven not to have peptic ulcer disease. DNA-DNA hybridization was performed with whole genomic probes made from an isolate from each of the three disease categories. Using a DNA probe from an isolate from a duodenal ulcer patient, we found that isolates from patients with duodenal ulcer and nonulcer gastritis yielded significant differences in levels of hybridization. The levels of hybridization of DNA from H. pylori isolates from duodenal ulcer patients, gastric ulcer patients, and nonulcer gastritis controls were 85.5% +/- 7%, 83% +/- 3%, and 78.3% +/- 5%, respectively (mean +/- SD), and the difference between the hybridization levels obtained with duodenal ulcer and nonulcer control target DNAs was statistically significant (P = 0.025). These data suggest that the outcome of infection (eg, ulcer or no ulcer) may be due to virulence factors encoded by genomic DNA. If such differences exist, it should be possible to produce probes that would identify the ulcer virulence gene(s) and clearly distinguish between ulcerogenic and nonulcerogenic strains of H. pylori.