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Helicobacter pylori resists phagocytosis by macrophages: quantitative assessment by confocal microscopy and
1Max-Planck-Institut für Infektionsbiologie, Abteilung Molekulare Biologie, 10117 Berlin, Germany.
Abstract:
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.
Insights
Helicobacter pylori bacteria prevent macrophages from engulfing them, a process crucial for immune defense. This bacterial immune evasion may explain persistent infections and related stomach diseases.
Area of Science:
- Microbiology
- Immunology
- Gastroenterology
Background:
- Helicobacter pylori infection causes stomach inflammation, potentially leading to ulcers and cancer.
- Immune cells infiltrate the stomach lining during H. pylori infection, contributing to mucosal damage.
Purpose of the Study:
- To investigate the interaction between Helicobacter pylori and phagocytic cells.
- To determine if H. pylori possesses mechanisms to evade immune cell uptake.
Main Methods:
- Utilized laser confocal microscopy and flow cytometry to analyze bacterial phagocytosis.
- Employed labeled bacteria and fluorescence quenching techniques for quantitative analysis.
- Used human and murine macrophages, along with the JOSKM myelomonocytic cell line.
Main Results:
- Helicobacter pylori actively inhibits its own phagocytosis by macrophages.
- This antiphagocytic activity extends to hindering the uptake of other bacteria, such as Neisseria gonorrhoeae (in trans effect).
- The cag pathogenicity island of H. pylori is essential for this immune evasion mechanism.
Conclusions:
- H. pylori exhibits a potent antiphagocytic activity, contributing to its persistence in the host.
- The identified immune escape strategy provides a model for studying persistent bacterial infections.
- Further research using cell lines and flow cytometry can advance understanding of H. pylori's interaction with the immune system.