Selective apoptosis during treatment with superantigen and lipopolysaccharide

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Studies of the events triggered by bacterial superantigens and lipopolysaccharide (LPS) provide rich insight into the constant battle between microbes and the oral immune system. In this study, we demonstrated a mechanism of apoptosis induced by staphylococcal enterotoxin B (SEB) in cultured monocytes and gingival fibroblasts, and some evidence for the anti-apoptotic function in CD80^+ monocytes. Apoptosis of monocytes was accelerated and enhanced by the addition of SEB. Increases in soluble CD95 ligand (sCD95L) levels were observed with stimulation with SEB, but not gamma interferon (IFN-γ). Our results clearly demonstrated that SEB treatment induces the activation of caspase-3 and -8, and pretreatment with zVAD-FMK, a broad inhibitor of caspases, prevented the induction of apoptosis at 24 h. Monocytes expressed constitutive NF-κB binding activity, and SEB further activated NF-κB, which was inhibited by pretreatment with pyrrolidine dithiocarbamate even at dose of 5 μM. PDTC markedly stimulated apoptosis induced by SEB and induced apoptosis in those treated with IFN-γ. Marked inhibition of the appearance of CD80^+ monocytes was achieved by treating cells with zVAD-FMK and DEVD-FMK, which was paralleled by reduced apoptosis of monocytes. LPS treatment resulted in significant reduction of the percentage of SEB-or IFN-γ induced apoptosis through induction of anti-apoptotic protein XIAP. Thus, our results indicated that SEB stimulation includes both anti-apoptotic actions through NF-κB activation and pro-apoptotic actions through sCD95L released by SEB, and that CD80 driven by NF-κB allows gingival tissues to participate in distinct survival programs.