Cristin-resultat-ID: 439695
Sist endret: 11. desember 2001 16:27
Resultat
Vitenskapelig artikkel
2001

Complement activation induced directly by Helicobacter pylori

Bidragsytere:
  • Audun Elnæs Berstad
  • Kolbjørn Høgåsen
  • Geir Bukholm
  • Anthony P. Moran og
  • Per Brandtzæg

Tidsskrift

Gastroenterology
ISSN 0016-5085
e-ISSN 1528-0012
NVI-nivå 2

Om resultatet

Vitenskapelig artikkel
Publiseringsår: 2001
Volum: 120
Sider: 1108 - 1116

Importkilder

ForskDok-ID: 60355

Beskrivelse Beskrivelse

Tittel

Complement activation induced directly by Helicobacter pylori

Sammendrag

Background and Aims: Helicobacter pylori is a frequent Gram-negative colonizer of the human stomach. Its interaction with complement may be involved in the pathogenesis of chronic gastritis, and was mechanistically studied in vitro. Methods: Four H. pylori strains, two cytotoxin associated gene (cag)A+ and two cagA-, were isolated from infected patients. Bacteria or purified H. pylori lipopolysaccharides were incubated with non-immune serum at 37°C; the activation products C3b/iC3b/C3c (C3bc) and terminal complement complex (TCC) were then quantified by immunoassays. The serum sensitivity of one strain (L01, cagA+) was tested by counting the numbers of colony-forming units. Results: All strains and lipopolysaccharides generated large amounts of C3bc and TCC. Blocking of the classical complement pathway by the calcium chelator ethylene glycol tetraacetic acid markedly reduced the complement products, suggesting that H. pylori and its lipopolysaccharides directly engage the classical activation pathway. H. pylori was shown to be serum-sensitive, but 30% or more non-immune serum was necessary to induce marked killing. After 5 min swelled bacteria coated with C3bc and TCC were demonstrated. Conclusions: H. pylori is complement-sensitive and activates the classical pathway even in the absence of specific antibodies. Released cell wall constituents such as lipopolysaccharides can activate complement and may explain why this bacterium induces gastric pathology without invading the mucosa.

Bidragsytere

Audun Elnæs Berstad

  • Tilknyttet:
    Forfatter
    ved Radiologisk, Ahus ved Universitetet i Oslo

Kolbjørn Høgåsen

  • Tilknyttet:
    Forfatter
    ved Immunologisk institutt ved Universitetet i Oslo

Geir Bukholm

  • Tilknyttet:
    Forfatter
    ved Universitetsadministrasjonen Ahus ved Universitetet i Oslo

Anthony P. Moran

  • Tilknyttet:
    Forfatter

Per Brandtzæg

  • Tilknyttet:
    Forfatter
    ved Patologiklinikken ved Universitetet i Oslo
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