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Helicobacter pylori
Relation between clinical presentation,Helicobacter pylori density, interleukin 1β and 8 production, and cagA status
  1. Y Yamaokaa,
  2. T Kodamab,
  3. M Kitac,
  4. J Imanishic,
  5. K Kashimab,
  6. D Y Grahama
  1. aDepartment of Medicine, Veterans Affairs Medical Centre and Baylor College of Medicine, Houston, Texas, USA, bThird Department of Internal Medicine, Kyoto Prefectural University of Medicine, Kyoto, Japan, cDepartment of Microbiology, Kyoto Prefectural University of Medicine, Kyoto, Japan
  1. Dr Y Yamaoka, Rm 3A320, Veterans Affairs Medical Centre (111D), 2002 Holcombe Blvd, Houston, TX 77030, USA.

Abstract

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

  • Abbreviations used in this paper

    DU
    duodenal ulcer
    IL
    interleukin
    MNC
    mononuclear cell
    PCR
    polymerase chain reaction
    PMN
    polymorphonuclear cell

    • https://doi.org/10.1136/gut.45.6.804

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    • Abbreviations used in this paper

      DU
      duodenal ulcer
      IL
      interleukin
      MNC
      mononuclear cell
      PCR
      polymerase chain reaction
      PMN
      polymorphonuclear cell
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      • Correction
        Correction for vol. 45, p. 804
        BMJ Publishing Group Ltd and British Society of Gastroenterology
        Gut 2000; 46 582-582 Published Online First: 01 Apr 2000.