Figure EV2. AMPKα1 in macrophages is not required for glucocorticoid‐dependent suppression of specific classical inflammatory gene expression and glucocorticoid receptor localization.

• A, B
  AMPKα1^fl/fl (WT) and LysM‐α1^−/− mice were exposed for 24 h to vehicle, lipopolysaccharide (LPS) or LPS + Dex treatment and (A) cytokines and (B) neutrophil numbers were quantified in BAL.
• C, D
  (C) Body mass and (D) body temperature curves for each group during survival experiment in Fig 3E.
• E
  RT–qPCR was performed on AMPKα1^fl/fl and LysM‐α1^−/− macrophages treated with LPS and Dex for 6 h.
• F
  WT and AMPKα1^−/− BMDMs were treated with Dex for 1 h and nuclear Glucocorticoid Receptor (GR) intensity determined by immunofluorescence was compared to cytoplasmic GR intensity.

Data information: results are means ± SEM or box and whiskers in which the central band represents the median of 5–9 (B), 13–15 (C, D), 3–7 (A, data below detection threshold were excluded from analysis) animals, and 3 (E, F) biological replicates. Statistical analysis by ANOVA (A, B) or ANOVA with repeated measures (C, D). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. ^$ P < 0.05, ^$$ P < 0.01, ^$$$ P < 0.001 vs untreated WT; ^£ P < 0.05 vs untreated LysM‐α1^−/− or AMPKα1^−/−, using one‐way ANOVA. Bar = 70 μm.