Mediators of Inflammation / 2018 / Article / Fig 2

Research Article

Epithelial Cells Attenuate Toll-Like Receptor-Mediated Inflammatory Responses in Monocyte-Derived Macrophage-Like Cells to Mycobacterium tuberculosis by Modulating the PI3K/Akt/mTOR Signaling Pathway

Figure 2

Mtb H37Rv-infected A549 cells inhibited the expression of TLR signaling of U937 cells in response to Mycobacteria infection. The coculture model of A549/U937 cells was infected with H37Rv Mycobacteria from the upper chamber (A549 cells, AI), lower chamber (U937 cells, UI), or both chambers (A549 and U937 cells, CI) at a MOI of 3 for 18 h before the U937 cells were harvested for analysis by RT-PCR assay. (a–g) Inductions of indicated transcripts of U937 cells infected with H37Rv in different conditions. (a) Fold of changes of TLR-2 transcripts over the noninfected cells; (B) fold of changes of TLR-4 transcripts over the noninfected cells; (c) fold of changes of TLR-6 transcripts over the noninfected cells; (d) fold of changes of TLR-8 transcripts over the noninfected cells; (e) fold of changes of MyD88 transcripts over the noninfected cells; (f) fold of changes of TRAF6 transcripts over the noninfected cells; (g) fold of changes of NF-κB transcripts over the noninfected cells. Error bars represent the standard deviation (SD) from three independent experiments. Compared to noninfection (NI) control, ; compared to infection of U937 cell alone, . NI: noninfected control; AI: infection was performed on A549 cell alone; UI: infection was performed on U937 alone; CI: infection was performed on both A549 cells and U937 cells.
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