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. 2020 Jan 27;11(1):68. doi: 10.1038/s41419-020-2263-0

Fig. 6. BCL-G regulates induction of pro-inflammatory chemokines by IFN-γ and TNF-α in human IEC.

Fig. 6

a–c HT-29 cells were stimulated with IFN-γ+TNF-α (1 or 10 ng/ml each) for 8 and 24 h. a Concentration of CXCL9, CXCL10, and CXCL11 measured in cell culture supernatants. b Concentration of CCL5 and CCL20 measured in cell culture supernatants. c Western blot showing levels of BCL-GL in HT-29 cells treated as indicated. d, e HT-29 cells transfected with a non-targeting siRNA (siCtrl) or siRNA targeting BCL-G (siBCL-G) were stimulated 48 h later with IFN-γ+TNF-α (1 or 10 ng/ml each) for 24 h. d Concentration of CXCL9, CXCL10 and CXCL11 measured in cell culture supernatants following BCL-G knockdown. e Concentration of CCL5 and CCL20 measured in cell culture supernatants following BCL-G knockdown. f Wild-type or BCL-G knockout (BCL-GKO) HT-29 cells were treated with IFN-γ+TNF-α (10 ng/ml each) for 24 h. Concentration of CCL5 and CCL20 measured in cell culture supernatants (left). Luminescent Cell-Titer Glo signal of wild-type and BCL-GKO HT-29 cells after 24 h culture (right). Data shown are the mean ± S.E.M. of at least n = 3 independent experiments. *p < 0.05, **p < 0.01 and ***p < 0.001 (two-way ANOVA followed by Tukey’s multiple comparisons test as indicated). NT — non-treated, wt — wild-type.