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HpaA is essential for Helicobacter pylori colonization in mice

Journal article
Authors Elisabet Carlsohn
Johanna Nyström
Ingrid Bölin
Carol L Nilsson
Ann-Mari Svennerholm
Published in Infect Immun
Volume 74
Issue 2
Pages 920-6
Publication year 2006
Published at Institute of Biomedicine, Department of Microbiology and Immunology
Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Pages 920-6
Language en
Links dx.doi.org/10.1128/IAI.74.2.920-926...
Keywords Adhesins, Bacterial/genetics/*metabolism, Animals, Bacterial Proteins/genetics/metabolism, Female, Gastric Mucosa/*microbiology, Gene Expression Profiling, Gene Expression Regulation, Bacterial, Helicobacter Infections/immunology/*microbiology, Helicobacter pylori/genetics/*growth & development/*pathogenicity, Humans, Mice, Mice, Inbred C57BL, Mutation, Proteome
Subject categories Microbiology in the medical area

Abstract

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.

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