Non-urease producing Helicobacter pylori in chronic gastritis

Background: Helicobacter pylori infection is the commonest cause of gastrit is. Different patterns of immune response to H. pylori infection and charac teristics of bacteria are considered to contribute to clinical outcomes. Aim: To determine characteristics of the host H. pylori relationship in sub jects with nonulcer dyspepsia and a histological diagnosis of gastritis. Methods: Thirty-five subjects with chronic gastritis undergoing endoscopy ( mean age 53 years, range 24-82, 14 male and 21 female) were studied, none o f whom was on nonsteroidal anti-inflammatory drugs or antibiotics. H. pylor i infection was determined by rapid urease test (CLOtest), culture, antibod y and RT-PCR for Ure C, Cag A and 26 kDa gene and histology. Cytokine produ ction of mucosal IL-6 and IL-8 were measured by ELISA. Results: Fifteen subjects were positive by CLOtest and/or bacterial culture . In these subjects histology showed numerous helical forms of H. pylori (G roup I). Nine subjects were negative by CLOtest, bacterial culture, and mRN A for urease C fragment, but positive by PCR for the 26 kDa protein encodin g gene. Histology in these subjects showed the presence of either coccoid f orms (four), or scant helical forms (two), or mixed coccoid/helical forms ( three) (Group II). Eleven subjects were negative by all methods of detectio n (Group III). IgG and IgA antibody levels in serum (p<0.05) and gastric ti ssue culture supernatant (p<0.001) were significantly higher in Group I tha n those in Group II or III. There were significant differences in the IgG s erum and IgA supernatant antibody levels (p<0.01 and p<0.05) when Group II was compared to Group III. Supernatant IL-6 levels were significantly highe r in Group I (p<0.01) than those from Groups II and III. IL-8 levels were h igher in Group I (p<0.01) and Group II (p<0.05) when compared to Group III. Conclusions: 'H. pylori-negative' gastritis can be associated with a non-ur ease producing form of H. pylori, with a reduction in both local and system ic antibody levels and mucosal pro-inflammatory cytokines.