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Infection and Immunity, August 2001, p. 5025-5030, Vol. 69, No. 8
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.8.5025-5030.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Differential Roles of Interleukin-18 (IL-18) and IL-12 for Induction of Gamma Interferon by Staphylococcal Cell Wall Components and Superantigens

Rogier J. L. Stuyt,1,2 Mihai G. Netea,1,2,* Soo-Hyun Kim,1 Daniela Novick,3 Menachem Rubinstein,3 Bart-Jan Kullberg,2 Jos W. M. Van der Meer,2 and Charles A. Dinarello1

Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado1; Department of Medicine, University Medical Center St. Radboud, Nijmegen, The Netherlands2; and Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel3

Received 20 February 2001/Returned for modification 26 March 2001/Accepted 16 May 2001

The roles of endogenous cytokines induced by either intact staphylococcal microorganisms or staphylococcal exotoxins were examined using human whole-blood cultures. To accomplish this, interleukin-18 binding protein (IL-18BP) and tumor necrosis factor binding protein (TNFbp) were used to neutralize IL-18 and TNF, respectively, whereas an anti-IL-12 monoclonal antibody was used to neutralize IL-12 and the IL-1 receptor antagonist (IL-1Ra) was used to block IL-1 receptors. Heat-killed Staphylococcus epidermidis and Staphylococcus aureus, as well as the staphylococcal superantigens toxic shock syndrome toxin-1 (TSST-1) and staphylococcus enterotoxin B (SEB) induced gamma interferon (IFN-gamma ) production. Staphylococcus spp.-induced production of IFN-gamma required the presence of endogenous IL-18, IL-12, and TNF. In contrast, TSST-1-induced IFN-gamma was not significantly reduced in the presence of IL-18BP, anti-IL-12 antibodies, IL-1Ra, or anti-TNFbp. SEB-induced IFN-gamma was significantly inhibited only by anti-IL-12 antibodies, indicating that endogenous IL-18, IL-1, and TNF are not required for SEB-induced IFN-gamma . In conclusion, the mechanisms of IFN-gamma stimulation by intact staphylococcal microorganisms and by exotoxins differ, and this is likely due to the different receptors which are triggered on the cell membranes. In contrast to its role in the interactions between staphylococci and host cells, IL-18 does not appear to play a major role in superantigen-induced IFN-gamma .

* Corresponding author. Mailing address: Department of Medicine (541), University Medical Center St. Radboud, Geert Grooteplein 8, P.O. Box 9101, 6500 HB Nijmegen, The Netherlands. Phone: 31-24-3614652. Fax: 31-24-3541734. E-mail: M.Netea{at}aig.azn.nl.

Infection and Immunity, August 2001, p. 5025-5030, Vol. 69, No. 8
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.8.5025-5030.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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