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 Fahy, O. L.
Right arrow Articles by McColl, S. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Fahy, O. L.
Right arrow Articles by McColl, S. R.

 Previous Article  |  Next Article 

Infection and Immunity, December 2006, p. 6885-6894, Vol. 74, No. 12
0019-9567/06/$08.00+0     doi:10.1128/IAI.01065-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

CXCL16 Regulates Cell-Mediated Immunity to Salmonella enterica Serovar Enteritidis via Promotion of Gamma Interferon Production{triangledown}

Olivier L. Fahy, Scott L. Townley, and Shaun R. McColl*

School of Molecular and Biomedical Science, University of Adelaide, Adelaide, South Australia, Australia

Received 6 July 2006/ Accepted 29 August 2006

CXCL16 is a recently discovered multifaceted chemokine that has been shown not only to recruit activated T lymphocytes but also to play a direct role in the binding and phagocytosis of bacteria by professional antigen-presenting cells. In this study, we investigated the role of CXCL16 in vivo in the regulation of the immune response using a murine model of Salmonella enterica serovar Enteritidis infection. The expression of CXCL16 was strongly upregulated in the spleens and livers of animals developing an immune response to a primary acute infection but not in the Peyer's patches. Animals developing a secondary response after reexposure to the bacteria displayed a similar pattern of expression. During the primary response, prior treatment with neutralizing antibodies to CXCL16 induced a significant increase in bacterial burden in the spleen and liver. The production of gamma interferon (IFN-{gamma}) by the lymphocytes in the spleen was decreased by anti-CXCL16 treatment. In comparison, during the secondary response, anti-CXCL16 treatment also significantly increased bacterial burden in both the spleen and liver but had no effect on IFN-{gamma} production. No role was found for CXCL16 in the production of antibody against SefA, a major surface antigen of S. enteritidis. Together, these results demonstrate a role for CXCL16 in the control of bacterial colonization of target organs and, more specifically, in the regulation of the cell-mediated arm of the primary response to S. enteritidis.

* Corresponding author. Mailing address: Department of Molecular and Biomedical Science, The University of Adelaide, North Terrace Campus, 5005, Adelaide, South Australia, Australia. Phone: 64 08-8303-4630. Fax: 64 08-8303-7532. E-mail: shaun.mccoll{at}adelaide.edu.au.

{triangledown} Published ahead of print on 18 September 2006.

Editor: F. C. Fang

Infection and Immunity, December 2006, p. 6885-6894, Vol. 74, No. 12
0019-9567/06/$08.00+0     doi:10.1128/IAI.01065-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Gonzalez-Juarrero, M., Kingry, L. C., Ordway, D. J., Henao-Tamayo, M., Harton, M., Basaraba, R. J., Hanneman, W. H., Orme, I. M., Slayden, R. A. (2009). Immune Response to Mycobacterium tuberculosis and Identification of Molecular Markers of Disease. Am. J. Respir. Cell Mol. Bio. 40: 398-409 [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»