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.
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