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Relation between clinical presentation,Helicobacter pylori density, interleukin 1β and 8 production, and cagA status


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
  • cagA
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  • Correction

    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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  • Correction
    BMJ Publishing Group Ltd and British Society of Gastroenterology