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. 2021 Jun 1;11:669989. doi: 10.3389/fcimb.2021.669989

Figure 1.

Figure 1

P.gingivalis induces immune senescence in murine bone marrow derived DCs (DCs): At day 6, DCs from young (yDCs) and old (oDCs) mice were co-cultured with P.gingivalis (10 MOI) ± Rapamycin (1µM), yDCs were treated with Dox (50nM) or P.gingivalis LPS (100ng/ml) and CS profiling was performed at day 8. (A) Representative western blot images for p16 INK4A, p53, and p21Waf1/Clip1 protein expression in BMDCS treated with P.gingivalis ± Rapamycin, Dox or LPS. (B) Densitometric analysis of p16 INK4A, p53, and p21Waf1/Clip1 protein expression in BMDCs. β-actin was used as a loading control. Band densities were normalized to β-actin, and data presented as fold change relative to the control (yDCs with no stimulus). (C) Representative images of SA-β-gal staining of BMDCs at PH 6, blue stain indicates senescence (D) Quantification of SA-β-gal positive cells using FACS analysis. (E) qPCR analysis showing relative mRNA expression of TNFa, IL-1β- and IL6 in BMDCs treated with P.gingivalis ± Rapamycin, Dox or LPS. Relative gene expression was calculated using delta-delta CT method and presented as fold change relative to the control (yDCs.). Analysis was done using one-way ANOVA and Tukey multiple comparison post hoc test (Data are expressed as means ± SD, *p<0.05, **p<0.01, ***p<0.001). NS, not significant.