Fig. 7.

NF-κB signaling is activated in response to meningitic PCN033 or RS218 and mediates the inflammatory response. a, b p65 phosphorylation and IκBα degradation were significantly enhanced upon challenge with PCN033 and RS218, as shown by western blotting and densitometry. c Nuclear translocation of the p65 subunit was apparent in the hBMECs upon infection with PCN033 and RS218, but barely observed in response to infection with HB101. d, e Real-time PCR analysis showed that meningitic E. coli strains PCN033- and RS218-induced proinflammatory cytokines production was significantly decreased via NF-κB signaling inhibition with 10 μM of BAY11-7082. Data were expressed as the mean ± standard deviation (mean ± SD) from three replicates or analyses. P < 0.05 (*) was considered statistically significant; p < 0.01 (**) and p < 0.001 (***) were extremely significant