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Infection and Immunity, April 2001, p. 2604-2611, Vol. 69, No. 4
Max-Planck-Institut für
Infektionsbiologie, Abteilung Molekulare Biologie, 10117 Berlin,
Germany
Received 19 September 2000/Returned for modification 1 November
2000/Accepted 27 November 2000
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.
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.4.2604-2611.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Helicobacter pylori Resists Phagocytosis
by Macrophages: Quantitative Assessment by Confocal Microscopy and
Fluorescence-Activated Cell Sorting
*
Corresponding author. Mailing address:
Max-Planck-Institut für Infektionsbiologie, Abteilung Molekulare
Biologie, Schumannstrasse 21/22, 10117 Berlin, Germany. Phone: 49 30 28 46 04 02. Fax: 49 30 28 46 04 01. E-mail:
meyer{at}mpiib-berlin.mpg.de.
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