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Figure 1 | BMC Molecular Biology

Figure 1

From: Glucocorticoids synergize with IL-1β to induce TLR2 expression via MAP Kinase Phosphatase-1-dependent dual Inhibition of MAPK JNK and p38 in epithelial cells

Figure 1

IL-1β up-regulates TLR2, but not TLR4, in human epithelial cells including primary bronchial epithelial cells. A, IL-1β up-regulates TLR2 mRNA, but not TLR4 mRNA, in HeLa cells in a time-dependent manner. Cells were treated with IL-1β (10 ng/ml) for the indicated time periods. The expression of TLR2 and TLR4 at mRNA level was then measured by real-time quantitative PCR in IL-1β-treated and -untreated human cervix epithelial HeLa cells. TLR2 and TLR4 mRNA levels were normalized to the level of cyclophilin that served as an internal control for the amount of RNA used in each reaction. Values are the mean ± SD; n = 3. The symbols (*) indicate results significantly different (p < 0.01) from unstimulated condition. B, IL-1β up-regulates TLR2 mRNA, but not TLR4 mRNA, in HeLa cells in a dose-dependent manner. HeLa cells were treated with the indicated concentration of IL-1β for 3 h. Values are the mean ± SD; n = 3. The symbols (*) indicate results significantly different (p < 0.01) from unstimulated condition. C, IL-1β up-regulates TLR2 mRNA, but not TLR4 mRNA, in primary human bronchial epithelial NHBE cells. NHBE cells were treated with IL-1β (10 ng/ml) for 3 h. Values are the mean ± SD; n = 3. The symbols (*) indicate results significantly different (p < 0.01) from unstimulated condition. D, IL-1β also induces expression of TLR2 at protein level in HeLa cells. HeLa cells were treated for 5 h with IL-1β (10 ng/ml). Protein level of TLR2 was then assessed by Western blot analysis using an anti-hTLR2 antibody. β-Actin was used as a protein loading control.

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