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 Thalmaier, U.
Right arrow Articles by Schneider-Brachert, W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Thalmaier, U.
Right arrow Articles by Schneider-Brachert, W.

 Previous Article  |  Next Article 

Infection and Immunity, June 2002, p. 3149-3155, Vol. 70, No. 6
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.6.3149-3155.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Role of Tumor Necrosis Factor Alpha in Helicobacter pylori Gastritis in Tumor Necrosis Factor Receptor 1-Deficient Mice

Ulrike Thalmaier,1 Norbert Lehn,1* Klaus Pfeffer,2 Manfred Stolte,3 Michael Vieth,3 and Wulf Schneider-Brachert1

Institute for Medical Microbiology and Hygiene, University of Regensburg, Regensburg,1 Institute for Medical Microbiology and Hygiene, Technical University of Munich, Munich,2 Institute of Pathology, Bayreuth, Germany3

Received 20 September 2001/ Returned for modification 10 December 2001/ Accepted 21 February 2002

Increased gastric production of interleukin 8 and tumor necrosis factor alpha (TNF-{alpha}) has been implicated in the pathogenesis of Helicobacter pylori-associated gastroduodenal disease. In the present study we used a mouse model to demonstrate whether loss of the tumor necrosis factor receptor 1 (TNF-R1) function leads to differences in gastric inflammation or the systemic immune response in H. pylori infection. Six different clinical isolates of H. pylori (three cytotoxin-positive and three cytotoxin-negative strains) were adapted to C57BL/6 mice. TNF-R1-deficient (TNF-R1-/-) mice (n = 19) and isogenetic controls (n = 24) were infected and sacrificed after 4 weeks of infection. Inflammation of the stomach and the humoral immune response to H. pylori were evaluated by histological, immunohistochemical, and serological methods. There was no detectable difference in the grade or activity of gastritis in TNF-R1-/- mice when they were compared with wild-type mice, but the number of lymphoid aggregates was slightly reduced in the gastric mucosa of TNF-R1-/- mice. Interestingly, total immunoglobulin G (IgG), as well as IgG1, IgG2b, and IgG3, H. pylori-specific antibody titers were significantly higher in wild-type mice. As revealed by immunoblot analysis, the difference in reactivity against H. pylori antigens was not based on a failure to recognize single H. pylori antigens in TNF-R1-/- mice. We therefore suggest that TNF-R1-mediated TNF-{alpha} signals might support a systemic humoral immune response against H. pylori and that the gastric inflammatory response to H. pylori infection seems to be independent of TNF-R1-mediated signals.

* Corresponding author. Mailing address: Institute for Medical Microbiology and Hygiene, University of Regensburg, Franz-Josef-Strauss-Allee 11, 93053 Regensburg, Germany. Phone: 49-941-944-6411. Fax: 49-941-944-6402. E-mail: norbert.lehn{at}klinik.uni-regensburg.de.

Editor: J. D. Clements

Infection and Immunity, June 2002, p. 3149-3155, Vol. 70, No. 6
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.6.3149-3155.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Algood, H. M. S., Cover, T. L. (2006). Helicobacter pylori Persistence: an Overview of Interactions between H. pylori and Host Immune Defenses. Clin. Microbiol. Rev. 19: 597-613 [Abstract] [Full Text]  
  • Kranzer, K., Sollner, L., Aigner, M., Lehn, N., Deml, L., Rehli, M., Schneider-Brachert, W. (2005). Impact of Helicobacter pylori Virulence Factors and Compounds on Activation and Maturation of Human Dendritic Cells. Infect. Immun. 73: 4180-4189 [Abstract] [Full Text]  
  • Thompson, L. J., Danon, S. J., Wilson, J. E., O'Rourke, J. L., Salama, N. R., Falkow, S., Mitchell, H., Lee, A. (2004). Chronic Helicobacter pylori Infection with Sydney Strain 1 and a Newly Identified Mouse-Adapted Strain (Sydney Strain 2000) in C57BL/6 and BALB/c Mice. Infect. Immun. 72: 4668-4679 [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»