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 Benjamin, M. A.
Right arrow Articles by McKay, D. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Benjamin, M. A.
Right arrow Articles by McKay, D. M.

 Previous Article  |  Next Article 

Infect Immun, May 1998, p. 2193-2199, Vol. 66, No. 5
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Changes in Murine Jejunal Morphology Evoked by the Bacterial Superantigen Staphylococcus aureus Enterotoxin B Are Mediated by CD4+ T Cells

Michelle A. Benjamin, Jun Lu, Graeme Donnelly, Parul Dureja, and Derek M. McKay*

Intestinal Disease Research Programme, McMaster University, Hamilton, Ontario, Canada L8N 3Z5

Received 29 October 1997/Returned for modification 12 January 1998/Accepted 4 February 1998

Bacterial superantigens (SAgs) are potent T-cell stimuli that have been implicated in the pathophysiology of autoimmune and inflammatory disease. We used Staphylococcus aureus enterotoxin B (SEB) as a model SAg to assess the effects of SAg exposure on gut form and cellularity. BALB/c, SCID (lacking T cells) and T-cell-reconstituted SCID mice were treated with SEB (5 or 100 µg intraperitoneally), and segments of the mid-jejunum were removed 4, 12, or 48 h later and processed for histochemical or immunocytochemical analysis of gut morphology and major histocompatibility complex class II (MHC II) expression and the enumeration of CD3+ T cells and goblet cells. Control mice received saline only. SEB treatment of BALB/c mice caused a time- and dose-dependent enteropathy that was characterized by reduced villus height, increased crypt depth, and a significant increase in MHC II expression. An increase in the number of CD3+ T cells was observed 48 h after exposure to 100 µg of SEB. Enteric structural alterations were not apparent in SEB-treated SCID mice compared to saline-treated SCID mice. In contrast, SEB challenge of SCID mice reconstituted with a mixed lymphocyte population or purified murine CD4+ T cells resulted in enteric histopathological changes reminiscent of those observed in SEB-treated BALB/c mice. These findings implicate CD4+ T cells in this SEB-induced enteropathy. Our results show that SAg immune activation causes significant changes in jejunal villus-crypt architecture and cellularity that are likely to impact on normal physiological processes. We speculate that the elevated MHC II expression and increased number of T cells could allow for enhanced immune responsiveness to other SAgs or environmental antigens.

* Corresponding author. Mailing address: Intestinal Disease Research Programme, HSC-3N5, Department of Pathology, McMaster University, 1200 Main St. W., Hamilton, Ontario, Canada L8N 3Z5. Phone: (905) 525-9140, ext. 22588. Fax: (905) 522-3454. E-mail: mckayd{at}fhs.McMaster.ca.

Infect Immun, May 1998, p. 2193-2199, Vol. 66, No. 5
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:

  • Heriazon, A., Zhou, P., Borojevic, R., Foerster, K., Streutker, C. J., Ng, T., Croitoru, K. (2009). Regulatory T Cells Modulate Staphylococcal Enterotoxin B-Induced Effector T-Cell Activation and Acceleration of Colitis. Infect. Immun. 77: 707-713 [Abstract] [Full Text]  
  • Pinchuk, I. V., Beswick, E. J., Saada, J. I., Suarez, G., Winston, J., Mifflin, R. C., Di Mari, J. F., Powell, D. W., Reyes, V. E. (2007). Monocyte Chemoattractant Protein-1 Production by Intestinal Myofibroblasts in Response to Staphylococcal Enterotoxin A: Relevance to Staphylococcal Enterotoxigenic Disease. J. Immunol. 178: 8097-8106 [Abstract] [Full Text]  
  • Perez-Bosque, A., Pelegri, C., Vicario, M., Castell, M., Russell, L., Campbell, J. M., Quigley, J. D. III, Polo, J., Amat, C., Moreto, M. (2004). Dietary Plasma Protein Affects the Immune Response of Weaned Rats Challenged with S. aureus Superantigen B. J. Nutr. 134: 2667-2672 [Abstract] [Full Text]  
  • Musch, M. W., Petrof, E. O., Kojima, K., Ren, H., McKay, D. M., Chang, E. B. (2004). Bacterial Superantigen-Treated Intestinal Epithelial Cells Upregulate Heat Shock Proteins 25 and 72 and Are Resistant to Oxidant Cytotoxicity. Infect. Immun. 72: 3187-3194 [Abstract] [Full Text]  
  • Savransky, V., Rostapshov, V., Pinelis, D., Polotsky, Y., Korolev, S., Komisar, J., Fegeding, K. (2003). Murine Lethal Toxic Shock Caused by Intranasal Administration of Staphylococcal Enterotoxin B. Toxicol Pathol 31: 373-378 [Abstract]  
  • Shupp, J. W., Jett, M., Pontzer, C. H. (2002). Identification of a Transcytosis Epitope on Staphylococcal Enterotoxins. Infect. Immun. 70: 2178-2186 [Abstract] [Full Text]  
  • Jedrzkiewicz, S., Kataeva, G., Hogaboam, C. M., Kunkel, S. L., Strieter, R. M., McKay, D. M. (1999). Superantigen Immune Stimulation Evokes Epithelial Monocyte Chemoattractant Protein 1 and RANTES Production. Infect. Immun. 67: 6198-6202 [Abstract] [Full Text]  
  • McKay, D. M., Lu, J., Jedrzkiewicz, S., Ho, W., Sharkey, K. A. (1999). Nitric Oxide Participates in the Recovery of Normal Jejunal Epithelial Ion Transport Following Exposure to the Superantigen, Staphylococcus aureus Enterotoxin B. J. Immunol. 163: 4519-4526 [Abstract] [Full Text]  
  • McKay, D. M., Benjamin, M. A., Lu, J. (1998). CD4+ T cells mediate superantigen-induced abnormalities in murine jejunal ion transport. Am. J. Physiol. Gastrointest. Liver Physiol. 275: G29-G38 [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»