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. 2018 Jan 19;9:2. doi: 10.3389/fimmu.2018.00002

Figure 3.

Figure 3

Phenolic glycolipids (PGLs) impair TLR4-mediated downstream signaling pathways. (A) Differential production of NO by bone marrow-derived macrophages (BMDMs) pretreated with 25 µM PGL-1 or vehicle (Veh) for 24 h prior to a 24 h stimulation with 1 µg/ml LPS + 100 U/ml IFN-γ, or 10 ng/ml TNF-α + 100 U/ml IFN-γ. ***P < 0.001, Mann–Whitney test, comparing PGL-1-treated to vehicle controls in each condition of cell stimulation. (B) Differential production of NO by wild-type, MyD88−/−, TRIFLps2/Lps2, or DKO BMDMs treated with 25 µM PGL-1 or vehicle (Veh) for 24 h prior to a 24 h stimulation with 1 µg/ml LPS + 100 U/ml IFN-γ. Controls include non-treated, non-stimulated cells (unstim). (C) Differential production of NO by MyD88−/− BMDMs treated with 25 µM PGL-bov, 25 µM PGL-1, 25 µM PGL-tb, or vehicle (Veh) for 24 h prior to a 24 h stimulation with LPS/IFN-γ. (D) Differential production of NO by MyD88−/− BMDMs infected with rBCG:no PGL, rBCG:PGL-bov, rBCG:PGL-tb, or rBCG:PGL-1 at a MOI of 5:1, or non-infected (no inf). In (B–D), data are mean NO levels ± SEM (n ≥ 3), expressed as fold changes relative to non-stimulated (unstim) or non-infected (no inf) controls. Data shown are from one experiment repeated twice with similar results. *P < 0.05, **P < 0.01, ***P < 0.001, repeated measures ANOVA with Tukey post hoc test, relative to vehicle or no PGL controls.