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Infection and Immunity, March 2001, p. 1256-1264, Vol. 69, No. 3
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.3.1256-1264.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Role of T Cells and Gamma Interferon during Induction of Hypersensitivity to Lipopolysaccharide by Toxic Shock Syndrome Toxin 1 in Mice

Martin M. Dinges and Patrick M. Schlievert*

Department of Microbiology, University of Minnesota Medical School, Minneapolis, Minnesota 55455

Received 30 May 2000/Returned for modification 11 August 2000/Accepted 20 November 2000

The superantigenic function of toxic shock syndrome toxin 1 (TSST-1) is generally regarded as an important determinant of its lethal effects in humans or experimental animals. This study examined the role of superantigenicity in a BALB/c mouse model of lethal TSST-1-induced hypersensitivity to lipopolysaccharide (LPS). In this model, TSST-1 greatly potentiated both LPS-induced lethality, as well as LPS-induced serum tumor necrosis factor alpha (TNF-alpha ) activity. Although BALB/c-SCID mice were resistant to these LPS enhancement effects of TSST-1, BALB/c-SCID mice reconstituted with T cells were completely susceptible to the enhancement effect of TSST-1 on LPS-induced serum TNF-alpha . Mice pretreated with cyclosporine (Cs) or neutralizing antibodies against gamma interferon (IFN-gamma ) did not develop lethal LPS hypersensitivity when injected with TSST-1, and these agents reduced the enhancement effect of TSST-1 on LPS-induced serum TNF-alpha by 99 and 85%, respectively. Cs pretreatment also completely inhibited the known capacity of TSST-1 to amplify LPS-induced levels of IFN-gamma in serum. In contrast, mice given Cs after a priming injection of TSST-1, but before LPS, still exhibited lethal hypersensitivity to LPS. Cs given after TSST-1 also did not inhibit enhancement of LPS-induced serum TNF-alpha by TSST-1 but inhibited the enhancement effect of TSST-1 on LPS-induced serum IFN-gamma by 50%. These experiments support the theory that TSST-1-induced hypersensitivity to LPS is mediated primarily by IFN-gamma derived from superantigen-activated T cells.

* Corresponding author. Mailing address: Department of Microbiology, University of Minnesota Medical School, 420 Delaware St., SE, Minneapolis, MN 55455. Phone: (612) 624-9471. Fax: (612) 626-0623. E-mail: pats{at}lenti.med.umn.edu.

Infection and Immunity, March 2001, p. 1256-1264, Vol. 69, No. 3
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.3.1256-1264.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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