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Infection and Immunity, August 2002, p. 4148-4157, Vol. 70, No. 8
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.8.4148-4157.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Mycobacterium bovis BCG-Infected Mice Are More Susceptible to Staphylococcal Enterotoxin B-Mediated Toxic Shock than Uninfected Mice despite Reduced In Vitro Splenocyte Responses to Superantigens{dagger}

João A. Pedras-Vasconcelos,1 Yvan Chapdelaine,1 Renu Dudani,1 Henk van Faassen,1 Dean K. Smith,1 and Subash Sad1,2*

Laboratory of Cellular Immunology, Institute for the Biological Sciences, National Research Council,1 Department of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, Ontario, Canada2

Received 14 December 2001/ Returned for modification 6 March 2002/ Accepted 17 May 2002

Type 1 T-cell responses against intracellular pathogens play a crucial role in mediating protection. We examined whether the induction of a strong type 1 T-cell response during a chronic bacterial infection influences responses to superantigens capable of inducing acute shock. Intravenous infection of mice with Mycobacterium bovis BCG appeared to induce a progressive anergy towards staphylococcal enterotoxin B (SEB) and towards antigen preparation of BCG (BCG-Ag) itself, based on diminished gamma interferon (IFN-{gamma}) production by SEB- and BCG-Ag-stimulated splenocytes from infected mice. In contrast to these in vitro results, injection of SEB into BCG-infected mice led to a dramatic increase in the serum IFN-{gamma} levels and the death of infected but not of control mice. In vitro hyporesponsiveness towards SEB and BCG-Ag occurred only with unfractionated splenocyte cultures, as purified T cells from infected mice produced higher levels of IFN-{gamma}. Hyporesponsiveness towards SEB and BCG-Ag in unfractionated splenocyte cultures was not due to suppressive antigen-presenting cells (APCs), as APCs from infected mice stimulated higher levels of IFN-{gamma} from purified T cells. The diminished IFN-{gamma} levels observed with bulk splenocytes appear to be due to changes in the T-cell-to-APC ratio that result in a decreased proportion of T cells, coupled to reduced proliferative responses and an increased susceptibility of effector T cells to activation-induced cell death in vitro. Our results indicate that the reported phenomena of T-cell anergy during mycobacterial infection may be an in vitro consequence of the development of a strong type 1 response in vivo.

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

{dagger} This is publication no. 42455 from the National Research Council of Canada.

Editor: R. N. Moore

Infection and Immunity, August 2002, p. 4148-4157, Vol. 70, No. 8
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.8.4148-4157.2002
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]  
  • 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]  
  • Chapdelaine, Y., Smith, D. K., Pedras-Vasconcelos, J. A., Krishnan, L., Sad, S. (2003). Increased CD8+ T Cell Memory to Concurrent Infection at the Expense of Increased Erosion of Pre-existing Memory: The Paradoxical Role of IL-15. J. Immunol. 171: 5454-5460 [Abstract] [Full Text]  


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