Inhibition of hBD-3, but not hBD-1 and hBD-2, mRNA expression by corticosteroids

Biochem Biophys Res Commun. 2001 Jan 19;280(2):522-5. doi: 10.1006/bbrc.2000.4157.

Abstract

Intensive use of corticosteroids may be accompanied by increased susceptibility to infections; hence, we investigated the effects of dexamethasone on the expression of antimicrobial peptides, termed human beta-defensins (hBD), by cultured bronchial epithelial cells and mononuclear phagocytes. The results revealed that dexamethasone inhibited the (stimulated) expression of mRNA for hBD-3, but not hBD-1 and hBD-2 by these epithelial cells. Dexamethasone did not affect the (stimulated) mRNA expression of hBD-1 and hBD-2 by mononuclear phagocytes, whereas these cells did not express hBD-3 mRNA.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adrenal Cortex Hormones / pharmacology*
  • Bronchi / cytology
  • Cells, Cultured
  • Dexamethasone / pharmacology
  • Epithelial Cells / drug effects
  • Epithelial Cells / metabolism
  • Epithelial Cells / microbiology
  • Gene Expression Regulation / drug effects*
  • Humans
  • Interferon-gamma / pharmacology
  • Interleukin-8 / metabolism
  • Lipopolysaccharides / pharmacology
  • Macrophages / drug effects
  • Macrophages / metabolism
  • Monocytes / drug effects
  • Monocytes / metabolism
  • Pseudomonas aeruginosa / physiology
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Streptococcus pneumoniae / physiology
  • Tumor Necrosis Factor-alpha / metabolism
  • beta-Defensins / genetics*

Substances

  • Adrenal Cortex Hormones
  • DEFB1 protein, human
  • DEFB4A protein, human
  • Interleukin-8
  • Lipopolysaccharides
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • beta-Defensins
  • Dexamethasone
  • Interferon-gamma