IGG SUBCLASS RESPONSE TO HELICOBACTER-PYLORI IN PATIENTS WITH CHRONIC ACTIVE GASTRITIS AND DUODENAL-ULCER

The IgG subclass response is determined by the type of bacteria producing the infection and by genetic factors of the host. Patients with a Helicobacter pylori infection develop a specific immune response that is mainly of the IgA and IgG class. We measured the IgG subclass response in 20 patients with chronic active gastritis without a history of duodenal ulcer and 20 patients with chronic active gastritis and duodenal ulcer diagnosed by endoscopy and histology. A control group included 20 H. pylori-negative patients and 60 H. pylori-positive blood transfusion donors. Systemic IgG subclass response was measured with a modified enzyme-linked immunosorbent assay technique, using as antigen a sonicate of six different H. pylori strains. Mouse monoclonal antibodies against each of the four human IgG subclasses (IgG1, IgG2, IgG3, and IgG4) were used. The total IgG anti-H. pylori antibody titres were equal in all three H. pylori-positive groups and significantly different from that of the negative control group (p < 0.01). The IgG subclass response in persons infected with H. pylori involved all four subclasses but was predominantly of the IgG1 and IgG2 subclasses. All of the groups with H. pylori infection had significantly higher levels of IgG1 than the negative control group, but no differences were detected among the three groups. However, the duodenal ulcer group had a significantly higher IgG2 response than the gastritis group (mean optical density +/- SEM, 0.382 +/- 0.047 versus 0.200 +/- 0.025, respectively; p < 0.05). In conclusion, we found a significant difference in IgG2 subclass antibody response against H. pylori bacteria between patients with chronic active gastritis without duodenal ulcer disease and patients with chronic active gastritis and duodenal ulcer diseases, suggesting a difference in either the genetically determined antibody response of the patients or the genetically encoded virulence factors in H. pylori, or both.