Changing glucocorticoid action: 11β-hydroxysteroid dehydrogenase type 1 in acute and chronic inflammation

Karen E. Chapman*, Agnes E. Coutinho, Zhenguang Zhang, Tiina Kipari, John S. Savill, Jonathan R. Seckl

*Corresponding author for this work

Research output: Contribution to journalLiterature reviewpeer-review


Since the discovery of cortisone in the 1940s and its early success in treatment of rheumatoid arthritis, glucocorticoids have remained the mainstay of anti-inflammatory therapies. However, cortisone itself is intrinsically inert. To be effective, it requires conversion to cortisol, the active glucocorticoid, by the enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). Despite the identification of 11β-HSD in liver in 1953 (which we now know to be 11β-HSD1), its physiological role has been little explored until recently. Over the past decade, however, it has become apparent that 11β-HSD1 plays an important role in shaping endogenous glucocorticoid action. Acute inflammation is more severe with 11β-HSD1-deficiency or inhibition, yet in some inflammatory settings such as obesity or diabetes, 11β-HSD1-deficiency/inhibition is beneficial, reducing inflammation. Current evidence suggests both beneficial and detrimental effects may result from 11β-HSD1 inhibition in chronic inflammatory disease. Here we review recent evidence pertaining to the role of 11β-HSD1 in inflammation.
Original languageEnglish
Pages (from-to)82-92
Number of pages11
JournalJournal of Steroid Biochemistry and Molecular Biology
Early online date19 Feb 2013
Publication statusPublished - Sep 2013


  • Glucocorticoid
  • mineralocorticoid
  • 11β-hydroxysteroid dehydrogenase
  • macrophage
  • inflammation
  • arthritis

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