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. 2020 Feb 4;17(4):498–509. doi: 10.7150/ijms.37833

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S100A8 and S100A9 induce the secretion of MCP-1, IL-6 and IL-8 through TLR4, PI3K, AKT, MAPKs and NF-κB in BEAS-2B cells. (A-B) BEAS-2B cells were pre-treated for 1 h with or without 5 μM TLR4i, 5 μM LY294002 (LY), 10 μM AKTi (AKT), 10 μM PD98059 (PD), 10 μM SB202190 (SB), 10 μM SP600125 (SP) and 2 μM BAY-11-7085 (BAY), after which the cells were incubated for 48 h in the absence or presence of 10 μg/mL S100A8 (A) and S100A9 (B). The supernatant (n=4) was collected and analyzed by ELISA. Data are expressed as the means ± SD and are presented relative to the control set at 100%. *p < 0.05 and **p < 0.01 indicate a significant difference between the control and S100A8- or S100A9-treated groups, and^##p < 0.01 and ^#p < 0.05 represent a significant difference between the S100A8- or S100A9-treated groups and the inhibitor-treated groups.

S100A8 and S100A9 induce the secretion of MCP-1, IL-6 and IL-8 through TLR4, PI3K, AKT, MAPKs and NF-κB in BEAS-2B cells. (A-B) BEAS-2B cells were pre-treated for 1 h with or without 5 μM TLR4i, 5 μM LY294002 (LY), 10 μM AKTi (AKT), 10 μM PD98059 (PD), 10 μM SB202190 (SB), 10 μM SP600125 (SP) and 2 μM BAY-11-7085 (BAY), after which the cells were incubated for 48 h in the absence or presence of 10 μg/mL S100A8 (A) and S100A9 (B). The supernatant (n=4) was collected and analyzed by ELISA. Data are expressed as the means ± SD and are presented relative to the control set at 100%. *p < 0.05 and **p < 0.01 indicate a significant difference between the control and S100A8- or S100A9-treated groups, and^##p < 0.01 and ^#p < 0.05 represent a significant difference between the S100A8- or S100A9-treated groups and the inhibitor-treated groups.