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Infection and Immunity, August 2005, p. 4643-4652, Vol. 73, No. 8
0019-9567/05/$08.00+0 doi:10.1128/IAI.73.8.4643-4652.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Max-Planck-Institut für Infektionsbiologie, Abt. Molekulare Biologie, Schumannstr. 20/21, D-10117 Berlin, Germany
Received 15 December 2004/ Returned for modification 21 January 2005/ Accepted 24 March 2005
Helicobacter pylori persistently infects the human stomach and can cause gastritis, gastric ulceration, and gastric cancer. The type IV secretion system (TFSS) of virulent H. pylori strains translocates the CagA protein, inducing the dephosphorylation of host cell proteins and leading to changes in the morphology or shape of AGS gastric epithelial cells. Furthermore, the TFSS is involved in the induction of proinflammatory cytokines. While the H. pylori genes required for TFSS function have been investigated systematically, little is known about possible host cell factors involved. We infected 19 different mammalian cell lines individually with H. pylori and analyzed CagA translocation, dephosphorylation of host cell proteins, chemokine secretion (interleukin-8 and macrophage inflammatory protein 2), and changes in cellular phenotypes. Our results demonstrate that not only bacterial but also host cell factors determine the cellular response to infection. The identification of such unknown host cell factors will add to our understanding of host-pathogen interactions and might help in the development of new therapeutic strategies.
Present address: University of Southern Denmark, Center for Experimental BioInformatics, Department of Biochemistry and Molecular Biology, Campusvej 55, DK-5230 Odense M, Denmark.
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