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. 2019 Jan 21;43(3):1430–1440. doi: 10.3892/ijmm.2019.4069

Figure 7.

Figure 7

FimA fusion protein induced an inflammatory response via the TLR4/NF-κB signaling pathway in PBMCs. (A) The expression levels of TLR4, NF-κB and MyD88 protein were detected by western blot analysis following treatment of PBMCs with 4 μg/ml FimA fusion protein with or without transfection with siTLR4 for 24 h. (B) Densitometric analysis of western blot data. (C) The expression levels of TLR4, NF-κB and MyD88 mRNA were detected by reverse transcription quantitative polymerase chain reaction following treatment of PBMCs with 4 μg/ml FimA fusion protein with or without transfection with siTLR4 for 24 h. Data are expressed as the means ± standard deviation based on at least three independent experiments. *P<0.05 vs. the control group (negative siRNA-transfected). TLR4, toll-like receptor 4; NF-κB; nuclear factor kappa-light-chain-enhancer of activated B cells; FimA, Porphyromonas gingivalis fimbriae; PBMC, peripheral blood mononuclear cells; MyD88, myeloid differentiation primary response 88; NF-κB p65, NF-κB p65 subunit; si, small interfering.