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. 2015 Mar 23;10(3):e0119235. doi: 10.1371/journal.pone.0119235

Fig 6. Inhibition of IRF3 and NF-κB affects early synthesis of IFN-β induced during Chlamydia infection.

Fig 6

(A) Bm1.1 cells were infected with 10 IFU/ cell C. muridarum up until the indicated time-points when the media was supplemented with either the IRF3 inhibitor BX-795, the NF-κB inhibitor JSH-23, or the solubilizing agent DMSO as a negative control. Cells were allowed to incubate in the presence of each inhibitor from the time indicated until cell supernatants were harvested at 24h PI, and IFN-β secreted was measured by ELISA. (B) C. muridarum-infected Bm1.11 cells were allowed to incubate in the presence of each inhibitor from the time indicated until cell supernatants were harvested at 24h PI, and IL-6 secreted was measured by ELISA. (C) Uninfected Bm1.11 cells were either DMSO-treated, transfected with 10, 25, or 50 μg/ml poly-IC, or transfected with poly-IC prior adding the inhibitors BX-795 and JSH-23 to the cells 1h post-transfection. IFN-β secreted into the supernatants 24 h post transfection was measured by ELISA. The results shown are representative of three independent experiments. * = p<0.05; ** = p< 0.01; NS = not statistically significant compared to poly-IC alone (C), or 24h C. muridarum infection control without inhibitor (A and B; denoted as MoPn).