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Infection and Immunity, April 2002, p. 1957-1964, Vol. 70, No. 4
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.4.1957-1964.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Preexisting Inflammation Due to Mycobacterium bovis BCG Infection Differentially Modulates T-Cell Priming against a Replicating or Nonreplicating Immunogen{dagger}

Renu Dudani,1 Yvan Chapdelaine,1 Henk van Faassen,1 Dean K. Smith,1 Hao Shen,2 Lakshmi Krishnan,1 and Subash Sad1,3*

Laboratory of Cellular Immunology, Institute for Biological Sciences, National Research Council,,1 Department of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, Ontario, Canada,3 Department of Microbiology, University of Pennsylvania School of Medicine, Hershey, Pennsylvania2

Received 20 September 2001/ Returned for modification 18 December 2001/ Accepted 10 January 2002

Induction of T-cell memory by vaccination ensures long-term protection against pathogens. We determined whether on-going inflammatory responses during vaccination influenced T-cell priming. A preexposure of mice to Mycobacterium bovis BCG impaired their subsequent ability to prime T cells against Listeria monocytogenes. This was characterized by a decrease in L. monocytogenes-specific gamma interferon (IFN-{gamma})-secreting CD4+ and CD8+ T cells. The intensity of T-cell priming towards L. monocytogenes depended on the extent of L. monocytogenes expansion, and a cessation of this expansion caused by M. bovis BCG-induced inflammation resulted in impairment in T-cell priming. A challenge of M. bovis BCG-infected mice with a higher L. monocytogenes dose increased L. monocytogenes survival and restored T-cell priming towards L. monocytogenes. Impairment in T-cell priming towards L. monocytogenes due to M. bovis BCG-induced inflammation resulted in a compromised protective efficacy in the long term after mice were rechallenged with L. monocytogenes. Preexisting inflammation selectively impaired T-cell priming for replicating immunogens as CD8+ T-cell response to ovalbumin administered as an inert antigen (ovalbumin-archaeosomes) was enhanced by M. bovis BCG preimmunization, whereas priming towards ovalbumin administered as a live immunogen (L. monocytogenes-ovalbumin) was impaired. Thus, depending on the nature of the immunogen, the presence of prior inflammatory responses may either impede or boost vaccine efficacy.

* Corresponding author. Mailing address: Institute for Biological Sciences, NRC, 100 Sussex Drive, Room 4105, Ottawa, Ontario, Canada K1A 0R6. Phone: 613 993 6015. Fax: 613 952 9092. E-mail: Subash.Sad{at}nrc.ca.

Editor: R. N. Moore

{dagger} This is publication no. 42444 from NRC.

Infection and Immunity, April 2002, p. 1957-1964, Vol. 70, No. 4
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.4.1957-1964.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Dudani, R., Murali-Krishna, K., Krishnan, L., Sad, S. (2008). IFN-{gamma} Induces the Erosion of Preexisting CD8 T Cell Memory during Infection with a Heterologous Intracellular Bacterium. J. Immunol. 181: 1700-1709 [Abstract] [Full Text]  
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  • van Faassen, H., Dudani, R., Krishnan, L., Sad, S. (2004). Prolonged Antigen Presentation, APC-, and CD8+ T Cell Turnover during Mycobacterial Infection: Comparison with Listeria monocytogenes. J. Immunol. 172: 3491-3500 [Abstract] [Full Text]  
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