Kayoko Abe

Flare-up reaction on murine contact hypersensitivity III. Effect of staphylococcal enterotoxin B

Staphylococcal enterotoxin B (SEB), a bacterial superantigen, is known as an immunomodulator because it activates an extremely large number of T-cells, and induces the production of large amounts of cytokines. In this study, we examined the effects of SEB on the contact hypersensitivity reaction (CHR). BALB/c mice were first sensitized through haptens applied to the back, and CHR was then induced through challenge to the left ear using the same haptens. SEB was administered intravenously 4 weeks later, causing a flare-up, peaking at 24 h post-administration, in the left ear that had previously exhibited CHR. This flare-up reaction was hapten non-specific, and was inhibited by anti-mouse tumor necrosis factor (TNF)-alpha antibodies. The flare-up was also suppressed by the oral administration of cyclosporin A prior to the administration of SEB. These results suggest that SEB induces a flare-up of CHR via the production of TNF-alpha.

SUPPRESSIVE EFFECT OF STAPHYLOCOCCAL ENTEROTOXIN B ON MURINE CONTACT HYPERSENSITIVITY

Superantigens (SAg) possess the capacity to interact with particular V beta regions of T cell receptor (TCR) and major histocompatibility complex (MHC) class II molecules, and activate a large number of T cells and accessory cells. staphylococcal enterotoxins (SEs) are recently well known as SAg and anticipate to modulate immunological reactions. In this study, we investigated the effect of staphylococcal enterotoxin B (SEB) on contact hypersensitivity reaction (CHR) to 2,4-dinitrofluorobenzene (DNFB) in BALB/c mice. SEB-injection inhibited the induction of sensitization on CHR. Suppressor cells were not found in the spleen or lymph node cells from mice treated with SEB. Normal spleen cells cultured with SEB showed significant proliferation and tumor necrosis factor-alpha (TNF-alpha) production. CHR was suppressed by intravenous injection of the culture supernatant. In addition, anti-TNF-alpha antibodies inhibited the suppressive effect induced by the supernatant. These findings indicate that TNF-alpha produced by SEB-responding cells inhibits the induction of sensitization on CHR. Therefore, SAg may play important roles in the modulation of immune system through the stimulation of TNF-alpha production.