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Infection and Immunity, February 2007, p. 1005-1016, Vol. 75, No. 2
0019-9567/07/$08.00+0     doi:10.1128/IAI.01176-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Identification of Helicobacter pylori Genes That Contribute to Stomach Colonization{triangledown} ,{dagger}

David N. Baldwin,1 Benjamin Shepherd,1 Petra Kraemer,1 Michael K. Hall,1 Laura K. Sycuro,1,2 Delia M. Pinto-Santini,1,2 and Nina R. Salama1,2*

Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, Washington,1 Program in Molecular and Cellular Biology, University of Washington, Seattle, Washington2

Received 26 July 2006/ Returned for modification 11 October 2006/ Accepted 2 November 2006

Chronic infection of the human stomach by Helicobacter pylori leads to a variety of pathological sequelae, including peptic ulcer and gastric cancer, resulting in significant human morbidity and mortality. Several genes have been implicated in disease related to H. pylori infection, including the vacuolating cytotoxin and the cag pathogenicity island. Other factors important for the establishment and maintenance of infection include urease enzyme production, motility, iron uptake, and stress response. We utilized a C57BL/6 mouse infection model to query a collection of 2,400 transposon mutants in two different bacterial strain backgrounds for H. pylori genetic loci contributing to colonization of the stomach. Microarray-based tracking of transposon mutants allowed us to monitor the behavior of transposon insertions in 758 different gene loci. Of the loci measured, 223 (29%) had a predicted colonization defect. These included previously described H. pylori virulence genes, genes implicated in virulence in other pathogenic bacteria, and 81 hypothetical proteins. We have retested 10 previously uncharacterized candidate colonization gene loci by making independent null alleles and have confirmed their colonization phenotypes by using competition experiments and by determining the dose required for 50% infection. Of the genetic loci retested, 60% have strain-specific colonization defects, while 40% have phenotypes in both strain backgrounds for infection, highlighting the profound effect of H. pylori strain variation on the pathogenic potential of this organism.

* Corresponding author. Mailing address: Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., Mailstop C3-168, P.O. Box 19024, Seattle, WA 98109-1024. Phone: (206) 667-1540. Fax: (206) 667-6524. E-mail: nsalama{at}fhcrc.org.

{triangledown} Published ahead of print on 13 November 2006.

Editor: V. J. DiRita

{dagger} Supplemental material for this article may be found at http://iai.asm.org/.

Infection and Immunity, February 2007, p. 1005-1016, Vol. 75, No. 2
0019-9567/07/$08.00+0     doi:10.1128/IAI.01176-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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