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. 2016 Dec 19;6:188. doi: 10.3389/fcimb.2016.00188

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Copyright © 2016 Mahapatra, Gallaher, Smith, Graham, Voth and Shaw.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Immunoblot analysis of C. burnetii modulation of NF-κB activation. (A) Top panel—immunoblot detection of phosphorylated RelA. Bottom panel—β-actin loading control. Uninfected THP-1 cells without Cm (U−Cm). Uninfected THP-1 cells with Cm (U+Cm). Infected THP-1 cells without Cm (I−Cm). Infected THP-1 cells with Cm (I+Cm). All samples were collected at 72 hpi. TNF-α-treated cells were used as positive controls for RelA phosphorylation. (B) Graph—difference in RelA protein phosphorylation levels relative to normalized β-actin. The Y-axis represents fold changes in phosphorylated RelA and the X axis indicates samples. Results represent the mean of three independent experiments. Error bars represent ± SD. Statistically significant differences between U−Cm and I−Cm or I+Cm are represented as ^*P ≤ 0.001—(Student's t-test).