Skip to main content
. 2019 Nov 3;2019:1603131. doi: 10.1155/2019/1603131

Figure 3.

Figure 3

Bcl-2 and Bcl-XL intracellular protein levels in PBMO and CMBO in response to infection, AREG stimulation, and inhibition of EGFR. Isolated monocytes were infected with E. coli, extracellular bacteria were removed, and the cells were cultivated for 24 h in medium supplemented with antibiotics. 1 h prior to infection, AREG stimulation and EGFR inhibitor treatment were started and maintained during the entire cultivation period. Quantification was performed by using flow cytometry. (a) Bcl-2 in PBMO and CBMO in response to infection and AREG stimulation. Bcl-2 levels are dose-dependently induced upon AREG stimulation in all settings. E. coli infection leads to an increase in Bcl-2 levels in CBMO but not in PBMO (n = 5). (b) Effect of EGFR inhibition on Bcl-2 in PBMO and CBMO in response to infection and AREG stimulation. AREG-mediated but not infection-mediated increase in Bcl-2 levels is suppressed by EGFR inhibition (n = 4). (c) Bcl-XL in PBMO and CBMO in response to infection and AREG stimulation. AREG stimulation dose-dependently increases Bcl-XL levels in both groups, while E. coli infection increases Bcl-XL solely in CBMO (n = 5). (d) Effect of EGFR inhibition on Bcl-XL levels in PBMO and CBMO in response to infection and AREG stimulation. AREG and infection-mediated increase in Bcl-XL levels is abolished by EGFR inhibition (n = 4). Data are shown as means + SD. Statistical significance was analyzed using two-way ANOVA with Bonferroni's multiple comparisons test. n.s.: not significant. ∗p < 0.05; ∗∗∗p < 0.005; and ∗∗∗∗p < 0.001.