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Figure 1 | Journal of Inflammation

Figure 1

From: Salivary histatin 3 inhibits heat shock cognate protein 70-mediated inflammatory cytokine production through toll-like receptors in human gingival fibroblasts

Figure 1

The effect of HSC70 on NF-κB-dependent activation through TLR2 and TLR4. (A) Luciferase assays for NF-κB-dependent activation by HSC70 through TLR4. 293-TLR4/MD2-CD14 cells were transfected with an NF-κB-dependent luciferase reporter plasmid (pIgκB-Luc). One day after transfection, cells were stimulated with heated and unheated E. coli LPS, BSA, HSP70, or HSC70 for 6 h. Cell lysates prepared from the stimulated cells were analyzed by luciferase assays. The values are shown as fold induction of the standardized luciferase activity over the unstimulated control (none). (B) Luciferase assays for NF-κB-dependent activation by the ATPase fragment of HSC70 in 293-TLR4/MD2-CD14 cells. The procedures were as in (A), except that the cells were stimulated with the heated or unheated HSC70 ATPase fragment. (C) Luciferase assays for NF-κB-dependent activation by HSC70 through TLR2. The procedures were as in (A), except that 293-TLR2/CD14 cells and P. gingivalis LPS were used. (D) Luciferase assays for NF-κB-dependent activation by the HSC70 ATPase fragment in 293-TLR2/CD14 cells. The procedures were as in (A and B). Bars represent the means and range of duplicate samples.

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