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Infection and Immunity, August 2001, p. 4891-4897, Vol. 69, No. 8
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.8.4891-4897.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Nickel-Responsive Induction of Urease Expression in Helicobacter pylori Is Mediated at the Transcriptional Level

Arnoud H. M. van Vliet,1,2,* Ernst J. Kuipers,2 Barbara Waidner,3 Beverly J. Davies,4 Nicolette de Vries,1,5,dagger Charles W. Penn,4 Christina M. J. E. Vandenbroucke-Grauls,1 Manfred Kist,3 Stefan Bereswill,3 and Johannes G. Kusters1,2

Department of Medical Microbiology, Faculty of Medicine, Vrije Universiteit,1 and Department of Gastroenterology, Vrije Universiteit Academic Hospital,5 Amsterdam, and Department of Gastroenterology and Hepatology, Academic Hospital Dijkzigt, Rotterdam,2 The Netherlands; Department of Microbiology, Institute of Medical Microbiology and Hygiene, University of Freiburg, Freiburg, Germany3; and School of Biosciences, University of Birmingham, Edgbaston, Birmingham, United Kingdom4

Received 18 December 2000/Returned for modification 9 February 2001/Accepted 4 May 2001

The nickel-containing enzyme urease is an essential colonization factor of the gastric pathogen Helicobacter pylori, as it allows the bacterium to survive the acidic conditions in the gastric mucosa. Although urease can represents up to 10% of the total protein content of H. pylori, expression of urease genes is thought to be constitutive. Here it is demonstrated that H. pylori regulates the expression and activity of its urease enzyme as a function of the availability of the cofactor nickel. Supplementation of brucella growth medium with 1 or 100 µM NiCl2 resulted in up to 3.5-fold-increased expression of the urease subunit proteins UreA and UreB and up to 12-fold-increased urease enzyme activity. The induction was specific for nickel, since the addition of cadmium, cobalt, copper, iron, manganese, or zinc did not affect the expression of urease. Both Northern hybridization studies and a transcriptional ureA::lacZ fusion demonstrated that the observed nickel-responsive regulation of urease is mediated at the transcriptional level. Mutation of the HP1027 gene, encoding the ferric uptake regulator (Fur), did not affect the expression of urease in unsupplemented medium but reduced the nickel induction of urease expression to only twofold. This indicates that Fur is involved in the modulation of urease expression in response to nickel. These data demonstrate nickel-responsive regulation of H. pylori urease, a phenomenon likely to be of importance during the colonization and persistence of H. pylori in the gastric mucosa.

* Corresponding author. Mailing address: Department of Gastroenterology and Hepatology, L448, Academic Hospital Dijkzigt, Dr. Molewaterplein 40, 3015 GD Rotterdam, The Netherlands. Phone: 31-10-4635946. Fax: 31-10-4634682. E-mail: vanvliet{at}mdl.azr.nl.

dagger Present address: Department of Gastroenterology and Hepatology, Academic Hospital Dijkzigt, Rotterdam, The Netherlands.

Infection and Immunity, August 2001, p. 4891-4897, Vol. 69, No. 8
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.8.4891-4897.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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