Glucocorticoid-Induced Leucine Zipper: A Promising Marker for Monitoring and Treating Sepsis

Front Immunol. 2020 Dec 16:11:606649. doi: 10.3389/fimmu.2020.606649. eCollection 2020.

Abstract

Sepsis is a clinical syndrome that resulting from a dysregulated inflammatory response to infection that leads to organ dysfunction. The dysregulated inflammatory response transitions from a hyper-inflammatory phase to a hypo-inflammatory or immunosuppressive phase. Currently, no phase-specific molecular-based therapies are available for monitoring the complex immune response and treating sepsis due to individual variations in the timing and overlap of the dysregulated immune response in most patients. Glucocorticoid-induced leucine zipper (GILZ), is broadly present in multiple tissues and circumvent glucocorticoid resistance (GCR) or unwanted side effects. Recently, the characteristics of GILZ downregulation during acute hyperinflammation and GILZ upregulation during the immunosuppressive phase in various inflammatory diseases have been well documented, and the protective effects of GILZ have gained attention in the field of sepsis. However, whether GILZ could be a promising candidate biomarker for monitoring and treating septic patients remains unknown. Here, we discuss the effect of GILZ in sepsis and sepsis-induced immunosuppression.

Keywords: anti-inflammatory; glucocorticoid-induced leucine zipper; glucocorticoids; sepsis; sepsis-induced immunosuppression.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / therapeutic use
  • Biomarkers / blood
  • Glucocorticoids / therapeutic use
  • Humans
  • Immunosuppressive Agents / therapeutic use
  • Predictive Value of Tests
  • Prognosis
  • Sepsis / blood*
  • Sepsis / diagnosis
  • Sepsis / drug therapy
  • Sepsis / immunology
  • Signal Transduction
  • Transcription Factors / blood*

Substances

  • Anti-Inflammatory Agents
  • Biomarkers
  • Glucocorticoids
  • Immunosuppressive Agents
  • TSC22D3 protein, human
  • Transcription Factors