Review of the molecular and cellular mechanisms of action of glucocorticoids for use in asthma

Shelby P. Umland*, Robert P. Schleimer, Sebastian L. Johnston

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

120 Scopus citations


Asthma is characterized by inflammation in the lung and glucocorticoids (GCs) are the most clinically effective treatment available. The success of chronic GC therapy for asthma stems largely from the ability of the GC-GC receptor (GR) complex to alter transcription of a wide array of molecules involved in the inflammatory process. Many of the adverse effects of elevated systemic GC levels have been reduced through the use of inhalation as a method of administration, as opposed to oral GC. GCs exert their effects by binding to the wild-type GR, GRα. The GRα complex can directly or indirectly alter gene transcription by binding to specific DNA sites or by activating transcription factors. There is also evidence to support GRα involvement in post-translational activities. In the management of asthma, the GRα down-regulates proinflammatory mediators such as interleukin-(IL)-1, 3, and 5, and up-regulates anti-inflammatory mediators such as IκB [inhibitory molecule for nuclear factor κB] IL-10, and 12. Newer GCs are being designed to increase potency and topical activity. Mometasone furoate (MF), has recently been developed for the treatment of asthma and inhibits key anti-inflammatory processes with a potency equal to or greater than that of fluticasone propionate. A better understanding of the molecular mechanisms involved might provide strategies for optimizing the effectiveness of GC in the treatment of asthma.

Original languageEnglish (US)
Pages (from-to)35-50
Number of pages16
JournalPulmonary Pharmacology and Therapeutics
Issue number1
StatePublished - Jan 1 2002


  • Asthma
  • Glucocorticoids
  • Mechanisms
  • Mometasone furoate
  • Transcription

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Biochemistry, medical
  • Pharmacology (medical)

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