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Infection and Immunity, August 2004, p. 4668-4679, Vol. 72, No. 8
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.8.4668-4679.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Chronic Helicobacter pylori Infection with Sydney Strain 1 and a Newly Identified Mouse-Adapted Strain (Sydney Strain 2000) in C57BL/6 and BALB/c Mice

Lucinda J. Thompson,1* Stephen J. Danon,1,2 John E. Wilson,1 Jani L. O'Rourke,1 Nina R. Salama,3 Stanley Falkow,4 Hazel Mitchell,1 and Adrian Lee1

School of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, New South Wales 2052,1 Molecular Science, CSIRO, North Ryde, New South Wales 1670, Australia,2 Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California 94305-5124,4 Fred Hutchinson Cancer Research Center, Seattle, Washington 98109-10243

Received 11 December 2003/ Returned for modification 8 March 2004/ Accepted 11 May 2004

The mouse model of Helicobacter pylori-induced disease using Sydney strain 1 (SS1) has been used extensively in Helicobacter research. Herein we describe the isolation and characterization of a new mouse-colonizing strain for use in comparative studies. One strain capable of persistent mouse colonization was isolated from a total of 110 clinical isolates and is named here SS2000 (Sydney strain 2000). Genome typing revealed a number of differences between SS1 and SS2000 as well as between them and the respective original clinical isolates. In particular, SS2000 lacked the entire cag pathogenicity island, while SS1 contained all 27 genes of the island. C57BL/6 and BALB/c mice were infected with SS1 or SS2000 or were treated with broth medium (controls). After 6 months host-specific effects were evident, including lower colonization levels in the BALB/c animals. Few pathological differences were observed between SS1- and SS2000-infected animals. However, by 15 months postinfection, SS1-infected C57BL/6 mice had developed more severe gastritis than the SS2000-infected animals. In contrast SS2000-infected BALB/c mice showed increased accumulation of mucosa-associated lymphoid tissue compared to those infected with SS1. This improved comparative model of H. pylori-induced disease allowed dissection of both host and strain effects and thus will prove useful in further studies.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, Stanford University School of Medicine, Fairchild Bldg. D300, 299 Campus Dr., Stanford, CA 94305. Phone: (650) 723-2671. Fax: (650) 723-1837. E-mail: lucindathompson{at}stanford.edu.

Editor: V. J. DiRita

Infection and Immunity, August 2004, p. 4668-4679, Vol. 72, No. 8
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.8.4668-4679.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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