On the other hand, the anti-apoptotic Bcl-2 was also upregulated, but this did not appear to be sufficient to ensure cell survival, as indicated by the apoptosis assays (Fig. 1, Fig.

2, Fig. 3, Fig. 4, Fig. 8). The upregulation of Bcl-2 is in agreement find more with Nakhjiri et al [16], underlining the fact that single molecule and single time point assessments alone can be misleading. Table 1 Apoptotic markers included

in the qPCR-Array shown Alvespimycin in Fig. 1. Genes 4SC-202 Killed Pg MOI:100 4 h Killed Pg MOI:100 24 h Live Pg MOI:100 4 h Live Pg MOI:100 24 h LTA 4.7 ± 3.4** 0.4 ± 0.1*** 1.1 ± 0.8* 3.8 ± 1.2** TNF 0.4 ± 0.01 2.0 ± 0.01** 2.1 ± 0.2*** 1.6 ± 0.1*** NFKB1 0.5 ± 0.01 1.4 ± 0.03 0.9 ± 0.1* 1.5 ± 0.05* TRADD 0.8 ± 0.01 1.5 ± 0.3** 0.9 ± 0.2 3.4 ± 0.1*** BID 0.7 ± 0.02 1.6 ± 0.1*** 0.9 ± 0.1* 3.1 ± 0.08*** CASP9 1.9 ± 0.7** 0.6 ± 0.2* 2.4 ± 1.1** 2.2 ± 0.2** CASP3 1.2 ± 0.02* 1.0 ± 0.01 1.2 ± 0.1* 2.2 ± 0.4*** BAX 1.5 ± 0.5* 1.0 ± 0.08 1.2 ± 0.01 1.7 ± 0.8** BCL2 0.9 ± 0.02** 0.7 ± 0.02** 0.9 ± 0.1** 1.2 ± 0.7* FADD 1.2 ± 0.01 1.0 ± 0.01 1.2 ± 0.1* 1.3 ± 0.05** RELA 0.9 ± 0.03** 1.2 ± 0.05** 1.1 ± 0.08* 1.5 ± 0.1*** ENDO-G

0.9 ± 0.01 1.0 ± 0.01 1.0 ± 0.1 1.3 ± 0.1** CHUK 0.9 ± 0.06* 1.2 ± 0.08** 1.1 ± 0.1* 1.2 ± 0.3** CASP8 0.9 ± 0.01** 1.0 ± 0.07 1.0 ± 0.1 1.1 ± 0.1** FASLG 1.3 ± 0.02 1.3 ± 0.02** 1.5 ± 0.1** 0.9 ± 0.2** DFFB 1.3 ± 0.03** 1.0 ± 0.1 1.2 ± 0.2* 0.8 ± 0.01 HGECs were challenged with live or heat-killed P. gingivalis 33277 at MOI:100 for 4 and 24 hours. Negative control was unchallenged HGECs in media. The data shown represent log-fold differences in gene expression (means ± SD) between the respective sample and the negative control. A value of 1 indicates no change, less than one indicates down-regulation and greater than one, up-regulation (*P < 0.05 ** P < 0.01, *** P < 0.001) It Inositol monophosphatase 1 has been suggested that apoptosis due to P. gingivalis challenge of human cells involves the gingipains [7, 8, 10, 11, 14]. Gingipains are cysteine proteases produced by P. gingivalis that are either secreted or membrane bound and arginine or lysine specific. In the present study, the mechanism used by P. gingivalis to induce apoptosis in gingival epithelial cells was shown to be dependent upon both Arg- and Lys- gingipains (Fig. 4). Gingipain deficient P. gingivalis mutants did not cause apoptosis as evidenced by a lack of DNA fragmentation indicating that gingipains are necessary for apoptosis to occur and that their depletion abolishes P.