<i>P. gingivalis</i> (Pg) LPS (PgLPS) and <i>E. coli</i> LPS activated the MAPK pathway in HGFs.

<p>Kinetics of P38 mitogen activated protein kinase (P38 MAPK), extracellular signal-regulated kinase1/2(ERK1/2), and Stress-activated protein kinase/c-Jun NH2-terminal kinase (SAPK/JNK) phosphorylation in HGFs are shown in <b>5.1</b>, <b>5.2</b> and <b>5.3</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 P38 MAPK, phospho-p38MAPK, ERK, phospho-ERK, JNK and phospho-JNK were determined by western blotting. Quantification of band intensities was performed by densitometry analysis using Image J software. The fold increase values of phospho-protiens of P38 MAPK (5.1D), ERK1/2 (5.2D) and SAPK/JNK (5.3D) as compared with the total protein are shown in the graphs (arbitrary units over control after normalization to the total protein). Equal loading was confirmed by stripping the immunoblot and re-probing it for α-Tubulin. 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.