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Infection and Immunity, February 2002, p. 771-778, Vol. 70, No. 2
0019-9567/01/$04.00+0     DOI: 70.2.771-778.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

In Vivo Complementation of ureB Restores the Ability of Helicobacter pylori To Colonize

Kathryn A. Eaton,1* Joanne V. Gilbert,2 Elizabeth A. Joyce,2,{dagger} Amy E. Wanken,1 Tracy Thevenot,1 Patrick Baker,1 Andrew Plaut,2 and Andrew Wright2

Department of Veterinary Biosciences, Ohio State University, Columbus, Ohio 43210,1 Departments of Molecular Biology and Microbiology and Medicine, Tufts University School of Medicine, Boston, Massachusetts 021112

Received 22 January 2001/ Returned for modification 13 March 2001/ Accepted 9 October 2001

The objective of this study was to determine (i) if complementation of ureB-negative Helicobacter pylori restores colonization and (ii) if urease is a useful reporter for promoter activity in vivo. Strains used were M6, M6{Delta}ureB, and 10 recombinant derivatives of M6 or M6{Delta}ureB in which urease expression was under the control of different H. pylori promoters. Mice were orally inoculated with either the wild type or one of the mutant strains, and colonization, in vivo urease activity, and extent of gastritis were determined. Of eight M6{Delta}ureB recombinants tested, four colonized mice. Of those, three had the highest in vitro urease activity of any of the recombinants, significantly different from that of the noncolonizing mutants. The fourth colonizing recombinant, with ureB under control of the cag-15 promoter, had in vitro urease activity which did not differ significantly from the noncolonizing strains. In vivo, urease activities of the four colonizing transformants and the wild-type control were indistinguishable. There were no differences in gastritis or epithelial lesions between mice infected with M6 and those infected with the transformants. These results demonstrate that recovery of urease activity can restore colonizing ability to urease-negative H. pylori. They also suggest that cag-15 is upregulated in vivo, as was previously suggested by demonstrating that it is upregulated upon contact with epithelial cells. Finally, our results suggest that total urease activity and colonization density do not contribute to gastritis due to H. pylori.

* Corresponding author. Mailing address: Department of Veterinary Biosciences, Ohio State University, 1925 Coffey Rd., Columbus, OH 43210. Phone: (614) 292-9667. Fax: (614) 292-6473. E-mail: eaton.1{at}osu.edu.

Editor: B. B. Finlay

{dagger} Present address: Stanford University School of Medicine, Stanford, CA 94305

Infection and Immunity, February 2002, p. 771-778, Vol. 70, No. 2
0019-9567/01/$04.00+0     DOI: 70.2.771-778.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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