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 Jedrzkiewicz, S.
Right arrow Articles by McKay, D. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Jedrzkiewicz, S.
Right arrow Articles by McKay, D. M.

 Previous Article  |  Next Article 

Infection and Immunity, November 1999, p. 6198-6202, Vol. 67, No. 11
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Superantigen Immune Stimulation Evokes Epithelial Monocyte Chemoattractant Protein 1 and RANTES Production

Sean Jedrzkiewicz,1 Galina Kataeva,1 Cory M. Hogaboam,2 Steven L. Kunkel,2 Robert M. Strieter,3 and Derek M. McKay1,*

Intestinal Disease Research Programme, McMaster University, Hamilton, Ontario, Canada,1 and Departments of Pathology2 and Internal Medicine,3 University of Michigan, Ann Arbor, Michigan

Received 11 June 1999/Accepted 29 June 1999

Bacterial superantigens (SAgs) have been implicated in inflammatory disease, and SAg-treated mice have increased jejunal T cells. Here we show that T84 cells (a human epithelial cell line) display increased MCP-1 and RANTES mRNA expression and protein production in response to conditioned medium from Staphylococcus aureus enterotoxin B (SEB; a model SAg)-activated immune cells. Also, MCP-1 and RANTES mRNAs were increased in jejunal enterocytes isolated from SEB-treated mice. We suggest that T-cell recruitment to the gut following SAg immune activation could be partially due to epithelium-derived chemokines.


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


Infection and Immunity, November 1999, p. 6198-6202, Vol. 67, No. 11
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.



This article has been cited by other articles:

  • 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]  
  • 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]  
  • Mennechet, F. J. D., Kasper, L. H., Rachinel, N., Li, W., Vandewalle, A., Buzoni-Gatel, D. (2002). Lamina Propria CD4+ T Lymphocytes Synergize with Murine Intestinal Epithelial Cells to Enhance Proinflammatory Response Against an Intracellular Pathogen. J. Immunol. 168: 2988-2996 [Abstract] [Full Text]  
  • ZHU, J., QIU, Y. S., MAJUMDAR, S., GAMBLE, E., MATIN, D., TURATO, G., FABBRI, L. M., BARNES, N., SAETTA, M., JEFFERY, P. K. (2001). Exacerbations of Bronchitis . Bronchial Eosinophilia and Gene Expression for Interleukin-4, Interleukin-5, and Eosinophil Chemoattractants. Am. J. Respir. Crit. Care Med. 164: 109-116 [Abstract] [Full Text]