GP induced band shifts, indicating binding of NFκB as well as of NFIL-6 to the corresponding DNA oligonucleotides (κ consensus, κ1, κ2, κ3 sites from the TNFα promoter; κ consensus from the IL-8 promoter; NFIL-6consensus from the IL-6 promoter; Table 1; Fig. 1A). The extent of the band shifts induced by GP was not statistically different when compared to LPS or TSST-1 (Fig. 1B). A supershift, conducted for an NFκB consensus site from the IL-8 promoter, demonstrated a GP-induced predominant binding of NFκB p65 and to a lesser degree of p50 (Fig. 1A). Accordingly, an immunoblot of nuclear extracts from GP-treated PBMC showed a strong binding of NFκB p65 and a weaker reaction of p50, whereas p52 was negative (Fig. 2). Simultaneous co-treatment of PBMC with GP did not change the LPS-induced NFκB binding to oligos from the TNFα promoter significantly (Fig. 1B), but substantially decreased the TSST-1-induced NFκB binding when compared to TSST-1 or GP (100 μg) and thus differed completely from the theoretical value of GP/TSST-1 calc. (n = 4; p < 0.05 vs. GP/TSST-1 calc. and p = 0.07 vs. TSST-1; Fig. 1B). GP was also able to induce band shifts indicative of binding of particular variants of NFAT to an oligo from the IFNγ promoter (Fig. 1A). An immunoblot for two NFAT subunits demonstrated a GP-induced binding of NFATc2 and to a lesser degree of NFATc1 (Fig. 2).