BACKGROUND It is not known whethercagA+ Helicobacter pylori in duodenal ulcer (DU) have enhanced virulence compared with non-DU cagA+ H pylori.
AIMS To investigate the relation between presentation, H pylori density, interleukin 1β (IL-1β) and IL-8 production, andcagA status.
METHODS Fifty DU and 50 gastritis patients with cagA+ H pylori and 11 with cagA− infections were studied. Bacterial density and cytokine production were assessed using the same biopsies. Cytokine production was also measured from supernatants of medium following coculture of H pylori with MKN-45 cells.
RESULTS There was no relation between H pylori density andcagA status. There was a dose dependent relation between mucosal cytokine levels and density ofcagA+ H pylori. H pylori density increased to a threshold, followed by a rapid increase in cytokines and then a plateau. IL-1β and IL-8 levels in the antrum were greater in DU than in gastritis; in the corpus the cytokine level/H pylori differed irrespective of similar H pylori densities. However, cytokine production was similar in vitro, independent of presentation or biopsy site, suggesting that host factors are critical determinants of the inflammatory response. Mucosal IL-8 and IL-1β levels were low withcagA− andcagA+, cagE− H pylori infections.
CONCLUSIONS The increase in antral IL-1β and IL-8 production and inflammation in DU is related to increased numbers of bacteria and not to an increase in cytokine production per cagA+ isolate. There was no evidence of enhanced virulence of H pylorifrom DU compared with cagA+ non-DUH pylori.
- duodenal ulcer
- Helicobacter pylori
- interleukin 1β
- interleukin 8
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An error occurred in the keys to figures 4 and 5 of the paper by Yamaoka et al (Gut 1999;45:804-11). Gastritis should be represented by open circles and duodenal ulcer by closed circles. We apologise for any confusion this error may have caused.
- Abbreviations used in this paper:
- duodenal ulcer
- mononuclear cell
- polymerase chain reaction
- polymorphonuclear cell
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