Helicobacter pylori resists phagocytosis by macrophages: quantitative assessment by confocal microscopy and fluorescence-activated cell sorting.

Helicobacter pylori infection of the stomach epithelium is characterized by an infiltration of polymorphonuclear and mononuclear cells. These immune cells contribute to mucosal damage which may eventually lead to gastritis, peptic ulcer, gastric cancer, and/or MALT-associated gastric lymphoma. Here we show that H. pylori inhibits its own uptake, as well as in trans the phagocytosis of Neisseria gonorrhoeae, by human and murine macrophages. This antiphagocytic activity is dependent on the presence of the cag pathogenicity island in the H. pylori genome. We demonstrate that H. pylori also expresses its antiphagocytic activity towards the myelomonocytic cell line JOSKM, thus providing a potent model for the study of the interaction between H. pylori and phagocytes. Our data were obtained using laser confocal microscopy and flow cytometry after quenching the fluorescence of labeled extracellular bacteria. The antiphagocytic activity of H. pylori may explain the persistence of H. pylori and its pathological consequences. The use of cell lines and flow cytometry will hopefully facilitate progress in our understanding of the immune escape of these persistent bacteria.