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. 2014 Mar 8;63(7):557–568. doi: 10.1007/s00011-014-0725-5

Fig. 2.

Fig. 2

PHA-543613 HCl inhibits P. gingivalis-induced expression of IL-8 by OKF6/TERT-2 oral keratinocytes through specific activation of α7nAChR. P. gingivalis-induced release of IL-8 by OKF6/TERT-2 oral keratinocytes was inhibited by the α7AChR agonist PHA-543613 HCl (a). The inhibition of release by the α7AChR agonist PHA-543613 HCl was mediated at the transcriptional level (b). The specific role of α7AChR in mediating the inhibition of P. gingivalis-induced expression and release of IL-8 was demonstrated using the specific antagonist, α-bungarotoxin (c). IL-8 release into bathing supernatants was determined by ELISA and changes in IL-8 mRNA expression by real-time PCR. ELISA data are presented as the mean IL-8 release with standard deviation (SD) and are derived from duplicate wells of 3 independent experiments (n = 3). Statistical analysis of ELISA data was performed by log transforming the data followed by ANOVA with a post hoc Bonferroni corrected t test (*P < 0.05). Real-time PCR data are presented as the fold induction change (±SD) in IL-8 mRNA expression in relation to the unstimulated control (2−ΔΔCT). The data are derived from duplicate wells of 3 independent experiments (n = 3). Statistical analysis of real-time PCR data was performed by Levene’s test of homoscedasticity on the natural log-transformed 2−∆CT values followed by an independent t test to compare two means (*P < 0.05)