European journal of gastroenterology & hepatology · 1995
Immunogenetic analysis of the human leukocyte antigen DQA1 locus in patients with duodenal ulcer or chronic atrophic gastritis harbouring Helicobacter pylori.
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Azuma T, Ito Y, Miyaji H, Dojyo M, Tanaka Y, Hirai M, Ito S, Kato T, Kohli Y
Аннотация
AIM: To examine the human leukocyte antigen (HLA)-DQA1 locus in patients harbouring Helicobacter pylori with chronic atrophic gastritis or duodenal ulcer as part of an investigation into immunogenetic differences in the host.
SUBJECTS AND METHODS: We examined 116 patients harbouring H. pylori (55 patients with chronic atrophic gastritis, 61 with duodenal ulcers) and 28 H. pylori-negative healthy controls for HLA-DQA1 genotypes. H. pylori infection was determined by culturing biopsy samples from the gastric body and antrum and by enzyme-linked immunosorbent assay. HLA-DQA1 typing was carried out by the polymerase chain reaction-restriction fragment length polymorphism method.
RESULTS: The allele frequency of DQA1*0102 was significantly higher in H. pylori-negative controls (0.250) than in H. pylori-positive duodenal ulcer patients (0.090). In contrast, the allele frequency of DQA1*0301 was significantly lower in H. pylori-negative controls (0.214) than in H. pylori-positive duodenal ulcer patients (0.418).
CONCLUSION: These results suggest that there are genetic differences in the HLA-DQA1 locus between H. pylori-positive duodenal ulcer patients and H. pylori-negative healthy controls.
SUBJECTS AND METHODS: We examined 116 patients harbouring H. pylori (55 patients with chronic atrophic gastritis, 61 with duodenal ulcers) and 28 H. pylori-negative healthy controls for HLA-DQA1 genotypes. H. pylori infection was determined by culturing biopsy samples from the gastric body and antrum and by enzyme-linked immunosorbent assay. HLA-DQA1 typing was carried out by the polymerase chain reaction-restriction fragment length polymorphism method.
RESULTS: The allele frequency of DQA1*0102 was significantly higher in H. pylori-negative controls (0.250) than in H. pylori-positive duodenal ulcer patients (0.090). In contrast, the allele frequency of DQA1*0301 was significantly lower in H. pylori-negative controls (0.214) than in H. pylori-positive duodenal ulcer patients (0.418).
CONCLUSION: These results suggest that there are genetic differences in the HLA-DQA1 locus between H. pylori-positive duodenal ulcer patients and H. pylori-negative healthy controls.