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 Eaton, K. A.
Right arrow Articles by Altman, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Eaton, K. A.
Right arrow Articles by Altman, E.

 Previous Article  |  Next Article 

Infection and Immunity, July 2004, p. 3925-3931, Vol. 72, No. 7
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.7.3925-3931.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Helicobacter pylori with a Truncated Lipopolysaccharide O Chain Fails To Induce Gastritis in SCID Mice Injected with Splenocytes from Wild-Type C57BL/6J Mice

K. A. Eaton,1* S. M. Logan,2 P. E. Baker,1 R. A. Peterson,1 M. A. Monteiro,2,{dagger} and E. Altman2

Department of Veterinary Biosciences, Ohio State University, Columbus, Ohio 43210,1 Institute for Biological Sciences, National Research Council of Canada, Ottawa, Ontario K1A OR6, Canada2

Received 9 December 2003/ Returned for modification 16 January 2004/ Accepted 9 March 2004

The goal of this study was to determine whether Helicobacter pylori lipopolysaccharide (LPS) O-chain polysaccharide contributes to gastritis in a mouse model. C57BL/6J or C57BL/6-Prkdcscid (severe combined immunodeficient [SCID]) mice were inoculated with H. pylori strain SS1 or SS1::0826kan, in which a ß-1,4-galactosyltransferase (HP0826), an LPS biosynthetic enzyme, had been disrupted. H. pylori strain SS1::0826kan expresses truncated LPS lacking O chain. Recipient SCID mice were given C57BL/6J splenocytes by intraperitoneal injection. Bacterial colonization, gastric lesions (gastritis, neutrophilic infiltration, and gastric epithelial metaplasia), cellular (delayed-type hypersensitivity) and humoral immune responses to H. pylori sonicate, and gastric gamma interferon (IFN-{gamma}) mRNA expression were quantified. Recipient SCID mice colonized by H. pylori strain SS1 developed extensive gastritis with loss of normal fundic gland morphology. In contrast, gastric mucosa of recipient SCID mice colonized by H. pylori strain SS1::0826kan was not statistically distinguishable from that of uninfected recipient mice. Delayed-type hypersensitivity and humoral immune responses were detected in infected mice inoculated with wild-type SS1, but not with SS1::0826kan. IFN-{gamma} transcription was lower in mice infected with SS1::0826kan than in mice infected with SS1. In this model of rapidly progressive gastritis due to H. pylori, the O chain contributed to the extent of gastritis and to the host immune response. These data support a role for H. pylori LPS O chain in direct induction of the host immune response leading to gastritis and gastric damage and are in contrast to protein antigens, such as urease and cag products which do not contribute to gastritis in mice.

* Corresponding author. Present address: Unit for Laboratory Animal Medicine, 018 Animal Research Facility, University of Michigan School of Medicine, 1150 W. Medical Center Dr., Ann Arbor, MI 48109-0614. Phone: (734) 936-3883. Fax: (734) 936-3235. E-mail: kateaton{at}med.umich.edu.

Editor: S. H. E. Kaufmann

{dagger} Present address: Department of Chemistry, University of Guelph, Guelph, Ontario N1G 2W1, Canada.

Infection and Immunity, July 2004, p. 3925-3931, Vol. 72, No. 7
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.7.3925-3931.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Keenan, J. I., Davis, K. A., Beaugie, C. R., McGovern, J. J., Moran, A. P. (2008). Alterations in Helicobacter pylori outer membrane and outer membrane vesicle-associated lipopolysaccharides under iron-limiting growth conditions. Innate Immunity 14: 279-290 [Abstract]  
  • Fox, J. G., Rogers, A. B., Whary, M. T., Ge, Z., Ohtani, M., Jones, E. K., Wang, T. C. (2007). Accelerated Progression of Gastritis to Dysplasia in the Pyloric Antrum of TFF2 / C57BL6 x Sv129 Helicobacter pylori-Infected Mice. Am. J. Pathol. 171: 1520-1528 [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]  
  • Ma, B., Simala-Grant, J. L., Taylor, D. E. (2006). Fucosylation in prokaryotes and eukaryotes. Glycobiology 16: 158R-184R [Abstract] [Full Text]  
  • Ma, B., Audette, G. F., Lin, S., Palcic, M. M., Hazes, B., Taylor, D. E. (2006). Purification, Kinetic Characterization, and Mapping of the Minimal Catalytic Domain and the Key Polar Groups of Helicobacter pylori {alpha}-(1,3/1,4)-Fucosyltransferases. J. Biol. Chem. 281: 6385-6394 [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»