GR Extinguishes Inflamed Chromatin, and NF-κB Evacuates Maria Fasolino, Golnaz Vahedi  Immunity  Volume 47, Issue 2, Pages 214-216 (August 2017) DOI: 10.1016/j.immuni.2017.07.025 Copyright © 2017 Elsevier Inc. Terms and Conditions

Figure 1 GR Activation Causes a Global Reduction in NF-κB Chromatin Binding, as well as Time-Dependent Transcriptional Effects (Left) When macrophages are treated with the glucocorticoid receptor (GR) agonist Dexamethasone (Dex) (#1) before stimulation with lipopolysaccharide (LPS) (#2), GRs translocate into the nucleus where they bind globally to chromatin. This activation of GRs leads to a genome-wide reduction in nuclear factor κB (NF-κB) chromatin binding via an unknown mechanism. GR activation before LPS stimulation additionally leads to an anti-inflammatory transcriptional response, especially the repression of inflammatory genes like cytokines and chemokines. (Right) When macrophages are first stimulated with LPS (#1) prior to treatment with Dex (#2), GR activation similarly leads to a genome-wide increase in GR chromatin binding and reduction in NF-κB chromatin binding. Additionally, GR activation after LPS similarly leads to an anti-inflammatory transcriptional response; however, metabolism-related genes are more repressed. Immunity 2017 47, 214-216DOI: (10.1016/j.immuni.2017.07.025) Copyright © 2017 Elsevier Inc. Terms and Conditions