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Amplified Host Defense by Toll-Like Receptor-Mediated Downregulation of the Glucocorticoid-Induced Leucine Zipper (GILZ) in Macrophages.

Front Immunol. 2019; 
Hoppstädter J, Diesel B, Linnenberger R, Hachenthal N, Flamini S, Minet M, Leidinger P, Backes C, Grässer F, Meese E, Bruscoli S, Riccardi C, Huwer H, Kiemer AK.
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Activation of toll-like receptors (TLRs) plays a pivotal role in the host defense against bacteria and results in the activation of NF-κB-mediated transcription of proinflammatory mediators. Glucocorticoid-induced leucine zipper (GILZ) is an anti-inflammatory mediator, which inhibits NF-κB activity in macrophages. Thus, we aimed to investigate the regulation and role of GILZ expression in primary human and murine macrophages upon TLR activation. Treatment with TLR agonists, e.g., Pam3CSK4 (TLR1/2) or LPS (TLR4) rapidly decreased GILZ mRNA and protein levels. In consequence, GILZ downregulation led to enhanced induction of pro-inflammatory mediators, increased phagocytic activity, and a higher capacity to kill... More


MyD88; NF-κB; TRIF; cytokine; inflammation; microRNA; nitric oxide; phagocytosis