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Infection and Immunity, February 2006, p. 920-926, Vol. 74, No. 2
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.2.920-926.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

HpaA Is Essential for Helicobacter pylori Colonization in Mice

Elisabet Carlsohn,^1*, Johanna Nyström,^2, Ingrid Bölin,² Carol L. Nilsson,^1,3 and Ann-Mari Svennerholm²

Department of Medical Biochemistry, Göteborg University, Box 440, 405 30 Göteborg, Sweden,¹ Department of Medical Microbiology and Immunology and Göteborg University Vaccine Research Institute, Göteborg University, Göteborg, Box 435, 405 30 Göteborg, Sweden,² National High Magnetic Field Laboratory, 1800 E. Paul Dirac Dr., Tallahassee, Florida 32310³

Received 6 July 2005/ Returned for modification 18 October 2005/ Accepted 10 November 2005

Infection with the human gastric pathogen Helicobacter pylori can give rise to chronic gastritis, peptic ulcer, and gastric cancer. All H. pylori strains express the surface-localized protein HpaA, a promising candidate for a vaccine against H. pylori infection. To study the physiological importance of HpaA, a mutation of the hpaA gene was introduced into a mouse-adapted H. pylori strain. To justify that the interruption of the hpaA gene did not cause any polar effects of downstream genes or was associated with a second site mutation, the protein expression patterns of the mutant and wild-type strains were characterized by two different proteomic approaches. Two-dimensional differential in-gel electrophoresis analysis of whole-cell extracts and subcellular fractionation combined with nano-liquid chromatography-Fourier transform ion cyclotron resonance mass spectrometry for outer membrane protein profiling revealed only minor differences in the protein profile between the mutant and the wild-type strains. Therefore, the mutant strain was tested for its colonizing ability in a well-established mouse model. While inoculation with the wild-type strain resulted in heavily H. pylori-infected mice, the HpaA mutant strain was not able to establish colonization. Thus, by combining proteomic analysis and in vivo studies, we conclude that HpaA is essential for the colonization of H. pylori in mice.

Editor: J. B. Bliska

E.C. and J.N. made equal contributions.

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