This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Terry, K.
Right arrow Articles by Ottemann, K. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Terry, K.
Right arrow Articles by Ottemann, K. M.

 Previous Article  |  Next Article 

Infection and Immunity, February 2005, p. 803-811, Vol. 73, No. 2
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.2.803-811.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Chemotaxis Plays Multiple Roles during Helicobacter pylori Animal Infection

Karianne Terry, Susan M. Williams, Lynn Connolly,{dagger} and Karen M. Ottemann*

Departments of Environmental Toxicology and Molecular, Cellular and Developmental Biology, University of California at Santa Cruz, Santa Cruz, California

Received 30 July 2004/ Returned for modification 28 September 2004/ Accepted 21 October 2004

Helicobacter pylori is a human gastric pathogen associated with gastric and duodenal ulcers as well as specific gastric cancers. H. pylori infects approximately 50% of the world's population, and infections can persist throughout the lifetime of the host. Motility and chemotaxis have been shown to be important in the infection process of H. pylori. We sought to address the specific roles of chemotaxis in infection of a mouse model system. We found that mutants lacking cheW, cheA, or cheY are all nonchemotactic and infect FVB/N mice with an attenuated phenotype after 2 weeks of infection. If infections proceeded for 6 months, however, this attenuation disappeared. Histological and culture analysis revealed that nonchemotactic mutants were found only in the corpus of the stomach, while the wild type occupied both the corpus and the antrum. Further analysis showed that nonchemotactic H. pylori isolates had an increased 50% infectious dose and were greatly outcompeted when coinfected with the wild type. If nonchemotactic mutants were allowed to establish an infection, subsequent infection with the wild type partially displaced the nonchemotactic mutants, indicating a role for chemotaxis in maintenance of infection. The data presented here support four roles for chemotaxis in H. pylori mouse infections: (i) establishing infection, (ii) achieving high-level infection, (iii) maintaining an infection when there are competing H. pylori present, and (iv) colonizing all regions of the stomach.

* Corresponding author. Mailing address: Department of Environmental Toxicology, University of California, Santa Cruz, 1156 High St. (ETOX), Santa Cruz, CA 95064. Phone: (831) 459-3482. Fax: (831) 459-3524. E-mail: ottemann{at}ucsc.edu.

Editor: D. L. Burns

{dagger} Present address: Division of Allergy and Infectious Diseases, University of Washington, Seattle, WA 98195.

Infection and Immunity, February 2005, p. 803-811, Vol. 73, No. 2
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.2.803-811.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Lowenthal, A. C., Hill, M., Sycuro, L. K., Mehmood, K., Salama, N. R., Ottemann, K. M. (2009). Functional Analysis of the Helicobacter pylori Flagellar Switch Proteins. J. Bacteriol. 191: 7147-7156 [Abstract] [Full Text]  
  • Pinto-Santini, D. M., Salama, N. R. (2009). Cag3 Is a Novel Essential Component of the Helicobacter pylori Cag Type IV Secretion System Outer Membrane Subcomplex. J. Bacteriol. 191: 7343-7352 [Abstract] [Full Text]  
  • Lowenthal, A. C., Simon, C., Fair, A. S., Mehmood, K., Terry, K., Anastasia, S., Ottemann, K. M. (2009). A fixed-time diffusion analysis method determines that the three cheV genes of Helicobacter pylori differentially affect motility. Microbiology 155: 1181-1191 [Abstract] [Full Text]  
  • Antunez-Lamas, M., Cabrera-Ordonez, E., Lopez-Solanilla, E., Raposo, R., Trelles-Salazar, O., Rodriguez-Moreno, A., Rodriguez-Palenzuela, P. (2009). Role of motility and chemotaxis in the pathogenesis of Dickeya dadantii 3937 (ex Erwinia chrysanthemi 3937). Microbiology 155: 434-442 [Abstract] [Full Text]  
  • Wen, Y., Feng, J., Scott, D. R., Marcus, E. A, Sachs, G. (2009). The pH-Responsive Regulon of HP0244 (FlgS), the Cytoplasmic Histidine Kinase of Helicobacter pylori. J. Bacteriol. 191: 449-460 [Abstract] [Full Text]  
  • Castillo, A. R., Woodruff, A. J., Connolly, L. E., Sause, W. E., Ottemann, K. M. (2008). Recombination-Based In Vivo Expression Technology Identifies Helicobacter pylori Genes Important for Host Colonization. Infect. Immun. 76: 5632-5644 [Abstract] [Full Text]  
  • Williams, S. M., Chen, Y.-T., Andermann, T. M., Carter, J. E., McGee, D. J., Ottemann, K. M. (2007). Helicobacter pylori Chemotaxis Modulates Inflammation and Bacterium-Gastric Epithelium Interactions in Infected Mice. Infect. Immun. 75: 3747-3757 [Abstract] [Full Text]  
  • Scott, D. R., Marcus, E. A., Wen, Y., Oh, J., Sachs, G. (2007). Gene expression in vivo shows that Helicobacter pylori colonizes an acidic niche on the gastric surface. Proc. Natl. Acad. Sci. USA 104: 7235-7240 [Abstract] [Full Text]  
  • Baldwin, D. N., Shepherd, B., Kraemer, P., Hall, M. K., Sycuro, L. K., Pinto-Santini, D. M., Salama, N. R. (2007). Identification of Helicobacter pylori Genes That Contribute to Stomach Colonization. Infect. Immun. 75: 1005-1016 [Abstract] [Full Text]  
  • Yao, J., Allen, C. (2006). Chemotaxis Is Required for Virulence and Competitive Fitness of the Bacterial Wilt Pathogen Ralstonia solanacearum.. J. Bacteriol. 188: 3697-3708 [Abstract] [Full Text]  
  • Croxen, M. A., Sisson, G., Melano, R., Hoffman, P. S. (2006). The Helicobacter pylori Chemotaxis Receptor TlpB (HP0103) Is Required for pH Taxis and for Colonization of the Gastric Mucosa.. J. Bacteriol. 188: 2656-2665 [Abstract] [Full Text]  
  • Logsdon, L. K., Mecsas, J. (2006). The Proinflammatory Response Induced by Wild-Type Yersinia pseudotuberculosis Infection Inhibits Survival of yop Mutants in the Gastrointestinal Tract and Peyer's Patches. Infect. Immun. 74: 1516-1527 [Abstract] [Full Text]  
  • Lane, M. C., Lockatell, V., Monterosso, G., Lamphier, D., Weinert, J., Hebel, J. R., Johnson, D. E., Mobley, H. L. T. (2005). Role of Motility in the Colonization of Uropathogenic Escherichia coli in the Urinary Tract. Infect. Immun. 73: 7644-7656 [Abstract] [Full Text]  
  • Jimenez-Pearson, M.-A., Delany, I., Scarlato, V., Beier, D. (2005). Phosphate flow in the chemotactic response system of Helicobacter pylori. Microbiology 151: 3299-3311 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»