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Microglia express functional 11 beta-hydroxysteroid dehydrogenase type 1.

Andres Gottfried-Blackmore1, Amanda Sierra, Bruce S McEwen

  • 1Laboratory of Neuroendocrinology, Rockefeller University, New York, New York 10065, USA.

Glia
|June 15, 2010
PubMed
Summary
This summary is machine-generated.

Microglia cells express 11 beta-hydroxysteroid dehydrogenase (11 beta HSD) Type 1, an enzyme that reduces inflammation by producing corticosterone. This finding reveals a potential self-regulatory mechanism in the brain

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Area of Science:

  • Neuroimmunology
  • Endocrinology
  • Molecular Biology

Background:

  • Glucocorticoids regulate inflammation via 11 beta-hydroxysteroid dehydrogenase (11 beta HSD) Type 1 and Type 2 enzymes.
  • Microglia are key immune cells in the central nervous system (CNS) and are implicated in neurodegeneration.
  • The role of 11 beta HSD enzymes in microglial inflammatory responses is not well understood.

Purpose of the Study:

  • To investigate the expression and activity of 11 beta HSD Type 1 and Type 2 in microglia.
  • To determine the role of these enzymes in regulating microglial inflammatory responses.

Main Methods:

  • Studied 11 beta HSD Type 1 and Type 2 expression in ex vivo FACS-sorted adult microglia and in vitro primary cultures.
  • Analyzed enzyme expression in lipopolysaccharide (LPS)-activated microglia.
  • Assessed the conversion of 11-dehydro-corticosterone to corticosterone (CORT) and its effect on cytokine production.

Main Results:

  • Microglia express 11 beta HSD-1 but not 11 beta HSD-2.
  • 11 beta HSD-1 expression is upregulated in LPS-activated microglia.
  • 11 beta HSD-1 activity generates CORT, which suppresses cytokine production in activated microglia.

Conclusions:

  • Microglia possess 11 beta HSD-1, enabling local glucocorticoid regulation.
  • 11 beta HSD-1 in microglia may serve as an intrinsic mechanism to inhibit neuroinflammation.
  • Targeting microglial 11 beta HSD-1 could offer therapeutic strategies for neurodegenerative diseases.