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. Author manuscript; available in PMC: 2019 Dec 12.
Published in final edited form as: Cell Host Microbe. 2018 Dec 12;24(6):791–803.e6. doi: 10.1016/j.chom.2018.11.001

Figure 1.

Figure 1.

RLR activation promotes glucose metabolism in macrophages. (A and B) Total metabolite profiling determined by LC-MS/MS metabolomics assay was assessed by principle component analysis (A) and pathway-enrichment analysis (B) in bone marrow-derived macrophages (BMMs) generated from C57BL/6 mice stimulated with vesicular stomatitis virus (VSV) (multiplicity of infection (MOI) = 1) for 4 h. (C) A summary of three glucose metabolic pathways, including the glycolysis (middle), PPP (left) and HBP (right). (D to G) Heatmap of metabolites (D) and fold changes in intermediate metabolites of the glycolysis (E), PPP (F), or HBP (G). (H) Fold change in 13C-labelled UDP-GlcNAc between non-treated and VSV-challenged BMMs in the presence of 13C6-glucose. (I) Immunoblotting (left) and densitometric analysis based on five independent experiments (right) to quantify ratio of total O-GlcNAc to actin in BMMs left untreated or treated with VSV or transfected with poly(I:C) (4 μg/ml) by lipofectamine 2000 for indicated periods. * P < 0.05, versus controls (two-tailed Student’s t-test (E to H)). Data are from one experiment representative of three experiments (A and B, D to G; mean ± s.d. of six biological replicates) or two experiments (H; mean ± s.d. of four biological replicates) or represent five independent experiments (I).