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Infection and Immunity, May 2008, p. 2235-2239, Vol. 76, No. 5
0019-9567/08/$08.00+0 doi:10.1128/IAI.01481-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Anna K. Walduck,1
Jason D. Price,1,2
John S. Pedersen,3
Nico van Rooijen,4
Martin J. Pearse,2,5
Odilia L. C. Wijburg,1,2,
* and
Richard A. Strugnell1,2,
Department of Microbiology and Immunology and the NHMRC Bacterial Pathogenesis Group, The University of Melbourne, Parkville, Victoria 3010, Australia,1 CRC for Vaccine Technology,2 Department of Anatomical Pathology, Alfred Hospital, Prahran, Victoria 3181, Australia,3 Department of Molecular Cell Biology, Vrije Universiteit VUMC, Amsterdam, The Netherlands,4 CSL Limited, Poplar Rd., Parkville, Victoria 3052, Australia5
Received 6 November 2007/ Returned for modification 2 January 2008/ Accepted 26 February 2008
Helicobacter pylori is the etiological agent of human chronic gastritis, a condition seen as a precursor to the development of gastrointestinal ulcers or gastric cancer. This study utilized the murine model of chronic H. pylori infection to characterize the role of macrophages in the induction of specific immune responses and gastritis and in the control of 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 spleens and stomachs 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.
Published ahead of print on 10 March 2008.
Present address: Department of Microbiology, Monash University, Melbourne, Australia.
Contributed equally as senior authors.
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