<i>P. gingivalis</i> (Pg) LPS₁₆₉₀ (PgLPS₁₆₉₀) and <i>E. coli</i> LPS activated the NF-κB pathway in HGFs.

<p>Kinetics of IκBα and NF-κB p65 phosphorylation in HGFs are shown in <b>4.1</b> and <b>4.2</b>, respectively. Cells were treated with PgLPS_1435/1449 (A), PgLPS₁₆₉₀ (B) and <i>E. coli</i> LPS (C) at 1 µg/mL for the indicated period of time. Cell extracts were prepared and the levels of IκBα, phospho-IκBα, NF-κB p65, phospho-NF-κB p65 were determined by western blotting. Equal loading, for each treatment, was confirmed by stripping away the immunoblot, then re-probing it for α-Tubulin. Quantification of band intensities was performed by densitometry analysis using Image J software. The values for fold increase of phospho- IκBα (4.1D) and Phospho-NF-κB p65 (4.2D) as compared with the total protein are shown in the graphs (arbitrary units over control after normalization to the total protein). The data shown here are from a representative experiment repeated three times with similar results<b>.</b> *Significant difference with a <i>p</i>-value <0.05 as compared with the controls without LPS treatment.