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. Author manuscript; available in PMC: 2010 Nov 1.

Published in final edited form as: Microb Pathog. 2009 Aug 26;47(5):258–266. doi: 10.1016/j.micpath.2009.08.004

TCDD does not inhibit the ingestion and intracellular multiplication of L. monocytogenes. A. TIB73 cells were pretreated with DMSO (), BNF (10 μM) (), or TCDD (10 nM) () for 5 h prior to infection with 10⁵ log-phase L. monocytogenes for 2 h (Ingestion). Cells were then washed extensively to remove extracellular Listeriae and incubated in media with 5 μg/mL gentamycin for 8 h. Cells were then lysed in sterile H₂O to determine the CFU of L. monocytogenes. B. Identically-treated and infected TIB73 cells were used to isolate total RNA for real-time RT-PCR analyses of CYP1A1. Data in A represent the mean±SEM Log₁₀CFU/mL of six independent experiments. *: p<0.05, as compared to the control. Data in B represent the fold change in CYP1A1 mRNA after TCDD or BNF treatment, after being normalized to the endogenous control (GAPDH).

Inline graphic — TCDD does not inhibit the ingestion and intracellular multiplication of L. monocytogenes. A. TIB73 cells were pretreated with DMSO (), BNF (10 μM) (), or TCDD (10 nM) () for 5 h prior to infection with 10⁵ log-phase L. monocytogenes for 2 h (Ingestion). Cells were then washed extensively to remove extracellular Listeriae and incubated in media with 5 μg/mL gentamycin for 8 h. Cells were then lysed in sterile H₂O to determine the CFU of L. monocytogenes. B. Identically-treated and infected TIB73 cells were used to isolate total RNA for real-time RT-PCR analyses of CYP1A1. Data in A represent the mean±SEM Log₁₀CFU/mL of six independent experiments. *: p<0.05, as compared to the control. Data in B represent the fold change in CYP1A1 mRNA after TCDD or BNF treatment, after being normalized to the endogenous control (GAPDH).