Serologic detection of infection with cagA+ Helicobacter pylori strains

Abstract

Approximately 60% of Helicobacter pylori isolates possess the cagA gene and express its 120-to 140-kDa product (CagA). In this study, the cagA gene was detected in H. pylori isolates from 26 (81.3%) of 32 patients with duodenal ulcers (DU), 17 (68.0%) of 25 patients with gastric ulcers, and 23 (59.0%) of 39 patients with nonulcer dyspepsia (NUD). By Western blotting (immunoblotting) with antiserum to CagA, in vitro CagA expression was demonstrated for 95.5% of cagA ؉ strains compared with 0% of strains lacking cagA. Sera from patients infected with cagA ؉ strains (n ‫؍‬ 66) reacted with recombinant CagA in an enzyme-linked immunosorbent assay to a significantly greater extent than either sera from patients infected with strains lacking cagA (n ‫؍‬ 30) or sera from uninfected persons (n ‫؍‬ 25) (P < 0.001). A strain lacking cagA was isolated from eight patients who had serum immunoglobulin G antibodies to CagA, which suggests that these patients were infected with multiple strains. Serum immunoglobulin G antibodies to CagA were present in 87.5, 76.0, and 56.4% of patients with DU, gastric ulcers, and NUD, respectively (odds ratio, 5.41; 95% confidence interval, 1.44 to 24.72; P ‫؍‬ 0.004 [DU versus NUD]). These data demonstrate an association between infection with cagA ؉ H. pylori and the presence of duodenal ulceration and indicate that serologic testing is a sensitive method for detecting infection with cagA ؉ strains.

Serologic Detection of CagA Positive Helicobacter pylori Infection in a Northern Italian Population: Its Association with Peptic Ulcer Disease

“…In this study, unlike the data previously reported [25,27], the magnitude of the anti-CagA titer (calculated by omitting subjects who were CagA negative but H. pylori positive) in DU patients was significantly higher than that of NUD patients. In contrast, no significant difference was observed between GU and NUD, even if GU patients showed anti-CagA titer higher than in NUD patients.…”

Augmented levels of gastric mucosal leucocyte activation by infection with cagA gene‐positive Helicobacter pylori

“…22,23 Anti-CagA antibodies in the serum and in the supernatants from gastric bioptic cultures have shown that CagA is produced in vivo 22,24,25 and that this protein is also detected more frequently in peptic ulcer patients than in patients with gastritis only. 22,24,26 There is also a high percentage of detection of anti-CagA antibodies in gastric cancer patients. 25 There is a growing body of evidence that the mucosal damage is partly caused by activation of leucocytes, with production of excessive amounts of ROM.…”

H. pylori and cagA: Relationships with Gastric Cancer, Duodenal Ulcer, and Reflux Esophagitis and Its Complications

“…The presence of the cagA gene (or the CagA protein) has been associated with both duodenal ulcer and gastric cancer [29][30][31][32]. Although the function of CagA is unknown, it is generally accepted that the presence of CagA identifies infection with organisms containing the cag pathogenicity island (CPI) [33] and is a marker for infection associated with a higher level of inflammation than caused by H. pylori without the pathogenicity island [34,35].…”