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Fig. 1 | Diabetology & Metabolic Syndrome

Fig. 1

From: The promotion of nephropathy by Porphyromonas gingivalis lipopolysaccharide via toll-like receptors

Fig. 1

TLR activation by P. gingivalis lipopolysaccharide (Pg)-LPS. The NF-κB activity on reporter and TLR-cotransfected HEK293 cells cultured with LPS was measured as the ratio of NF-κB-dependent firefly luciferase activity to β-actin promoter-dependent Renilla luciferase activity. For the TLR2/1-specific NF-κB activation (left panel), the synthetic tripalmitoyl-S-glyceryl-cysteine (Pam3CSK4; TLR1/2 agonist, InvivoGen) showed the highest activity among all the chemicals tested. The Pg-LPS from Invivogen, Pg-LPS from Wako, and LPS obtained from P. gingivalis cultured with hemin at high and low concentrations (Pg-Lo Hemin and Pg-Hi Hemin) were lower and of similar intensity. The E. coli LPS (E. coli LPS) and LPS consisting of tetra-acylated lipid A structures (Pg1435) showed the lowest activity among all the chemicals tested for the host response via TLR2/1. For the TLR4-specific NF-κB activation (right panel), E. coli LPS (E. coli LPS) showed the highest activity among all the chemicals tested. The Pg-LPS from Invivogen, Pg-LPS from Wako, LPS obtained from P. gingivalis cultured with hemin at high and low concentrations (Pg-Lo Hemin and Pg-Hi Hemin), and LPS consisting of tetra-acylated lipid A structures (Pg1435) form an extremely low activity group, and the synthetic tripalmitoyl-S-glyceryl-cysteine (Pam3CSK4) also showed little activity. Experiments were repeated five times and statistically analyzed. There were significantly differences between Pam3CSK4 and others in TLR2/1 activation, and between E. coli LPS and others in TLR4 activation by ANOVA

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