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Infection and Immunity, June 2002, p. 2846-2852, Vol. 70, No. 6
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.6.2846-2852.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

NikR Mediates Nickel-Responsive Transcriptional Induction of Urease Expression in Helicobacter pylori

Arnoud H. M. van Vliet,1* Sophie W. Poppelaars,1 Beverly J. Davies,2 Jeroen Stoof,1 Stefan Bereswill,3 Manfred Kist,3 Charles W. Penn,2 Ernst J. Kuipers,1 and Johannes G. Kusters1

Department of Gastroenterology and Hepatology, Erasmus Medical Center, Rotterdam, The Netherlands,1 School of Biosciences, University of Birmingham, Birmingham, United Kingdom,2 Department of Medical Microbiology and Hygiene, Institute ofMedical Microbiology and Hygiene, University Hospital of Freiburg, Freiburg, Germany3

Received 12 November 2001/ Returned for modification 5 February 2002/ Accepted 19 February 2002

The important human pathogen Helicobacter pylori requires the abundant expression and activity of its urease enzyme for colonization of the gastric mucosa. The transcription, expression, and activity of H. pylori urease were previously demonstrated to be induced by nickel supplementation of growth media. Here it is demonstrated that the HP1338 protein, an ortholog of the Escherichia coli nickel regulatory protein NikR, mediates nickel-responsive induction of urease expression in H. pylori. Mutation of the HP1338 gene (nikR) of H. pylori strain 26695 resulted in significant growth inhibition of the nikR mutant in the presence of supplementation with NiCl2 at >=100 µM, whereas the wild-type strain tolerated more than 10-fold-higher levels of NiCl2. Mutation of nikR did not affect urease subunit expression or urease enzyme activity in unsupplemented growth media. However, the nickel-induced increase in urease subunit expression and urease enzyme activity observed in wild-type H. pylori was absent in the H. pylori nikR mutant. A similar lack of nickel responsiveness was observed upon removal of a 19-bp palindromic sequence in the ureA promoter, as demonstrated by using a genomic ureA::lacZ reporter gene fusion. In conclusion, the H. pylori NikR protein and a 19-bp operator sequence in the ureA promoter are both essential for nickel-responsive induction of urease expression in H. pylori.

* Corresponding author. Mailing address: Department of Gastroenterology and Hepatology, Room L-481, Erasmus Medical Center, Dr. Molewaterplein 40, 3015 GD Rotterdam, The Netherlands. Phone: 31-10-4635946. Fax: 31-10-4634682. E-mail: vanvliet{at}mdl.azr.nl.

Editor: R. N. Moore

Infection and Immunity, June 2002, p. 2846-2852, Vol. 70, No. 6
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.6.2846-2852.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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