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 5

Impact of PI3K signaling in U937 cells in response to H37Rv infection. In the presence or absence of PI3K inhibitor LY294002, 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 culture medium and U937 cells were harvested for analysis by RT-PCR assay. Inductions of indicated transcripts of U937 cells infected with Mtb H37Rv in different conditions. The data was presented as the fold of changes of indicated transcripts over the noninfected cells. The ability of A549 cell-mediated reduction of TLR-mediated inflammations in U937 cells was reversed by the addition of LY294002. Error bars represent the standard deviation (SD) from three independent experiments. Compared to noninfection (NI) control, and ; compared to the absence of LY294002, and . 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.