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Infect. Immun. doi:10.1128/IAI.01481-07
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Macrophages are mediators of gastritis in acute Helicobacter pylori infection in C57BL/6 mice

Department of Microbiology and Immunology and the NHMRC Bacterial Pathogenesis Group, The University of Melbourne, Parkville VIC 3010, Australia; CRC for Vaccine Technology; Department of Anatomical Pathology, Alfred Hospital, Prahran VIC 3181, Australia; Department of Molecular Cell Biology, Vrije Universiteit VUMC, Amsterdam, The Netherlands. CSL Limited, Poplar Rd, Parkville VIC 3052, Australia

^* To whom correspondence should be addressed. Email: odilia{at}unimelb.edu.au.

	Abstract

Helicobacter pylori is the aetiological agent of human chronic gastritis, a condition seen as a precursor to the development of gastrointestinal ulcers or gastric cancer. This study utilised the murine model of chronic H. pylori infection to characterize the role of macrophages in the induction of specific immune responses, gastritis and in controlling the bacterial burden following H. pylori infection and vaccination. Drug-loaded liposomes were injected intravenously to deplete macrophages from C57BL/6 mice and effective removal of CD11b⁺ cells from the spleen and stomach of mice was confirmed by immunofluorescence microscopy. Transient elimination of macrophages from C57BL/6 mice during the early period of infection reduced the gastric pathology induced by H. pylori SS1 but did not affect the bacterial load in the stomach. These data suggest that macrophages are important to the severity of gastric inflammation during H. pylori infection. (136)