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Infection and Immunity, September 1998, p. 4517-4521, Vol. 66, No. 9
Unité de Pathogénie
Bactérienne des Muqueuses, Institut Pasteur, 75724 Paris Cedex
15, France
Received 4 March 1998/Returned for modification 20 April
1998/Accepted 24 June 1998
We produced defined isogenic Helicobacter pylori ureI
mutants to investigate the function of UreI, the product of one of the genes of the urease cluster. The insertion of a cat
cassette had a strong polar effect on the expression of the downstream
urease genes, resulting in very weak urease activity. Urease activity, measured in vitro, was normal in a strain in which ureI was
almost completely deleted and replaced with a nonpolar cassette. In
contrast to previous reports, we thus found that the product of
ureI was not necessary for the synthesis of active urease.
Experiments with the mouse-adapted H. pylori SS1
strain carrying the nonpolar ureI deletion showed that UreI
is essential for H. pylori survival in vivo and/or
colonization of the mouse stomach. The replacement of ureI
with the nonpolar cassette strongly reduced H. pylori survival in acidic conditions (1-h incubation in phosphate-buffered saline solution at pH 2.2) in the presence of 10 mM urea. UreI is
predicted to be an integral membrane protein and may therefore be
involved in a transport process essential for H. pylori survival in vivo.
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
The Helicobacter pylori UreI Protein Is
Not Involved in Urease Activity but Is Essential for Bacterial Survival
In Vivo
*
Corresponding author. Mailing address: Unité de
Pathogénie Bactérienne des Muqueuses, Institut Pasteur, 28 rue du Dr. Roux, 75724 Paris Cedex 15, France. Phone: 33 1 40 61 32 73. Fax: 33 1 40 61 36 40. E-mail: hdereuse{at}pasteur.fr.
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