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Infection and Immunity, May 2006, p. 3052-3059, Vol. 74, No. 5
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.5.3052-3059.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Requirement of Histidine Kinases HP0165 and HP1364 for Acid Resistance in Helicobacter pylori

John T. Loh1 and Timothy L. Cover1,2,3*

Departments of Medicine,1 Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee 37232,2 Veterans Affairs Medical Center, Nashville, Tennessee 372123

Received 9 November 2005/ Returned for modification 22 December 2005/ Accepted 6 February 2006

In this study, we investigated a potential requirement of two-component signal transduction systems for acid resistance in Helicobacter pylori. In comparison to a wild-type strain, isogenic strains with null mutations in either HP0165 or HP1364 histidine kinases were impaired in their ability to grow at pH 5.0. The growth of complemented mutant strains was similar to that of the wild-type strain. H. pylori DNA array analyses and transcriptional reporter assays indicated that acid-responsive gene transcription was altered in the HP0165 and HP1364 null mutant strains compared to the parental wild-type strain. These results indicate that intact HP0165 and HP1364 histidine kinases are required for acid resistance in H. pylori.

* Corresponding author. Mailing address: Division of Infectious Diseases, A2200 Medical Center North, Vanderbilt University School of Medicine, Nashville, TN 37232. Phone: (615) 322-2035. Fax: (615) 343-6160. E-mail: timothy.L.cover{at}vanderbilt.edu.

Editor: V. J. DiRita

Infection and Immunity, May 2006, p. 3052-3059, Vol. 74, No. 5
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.5.3052-3059.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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