Psychological stress regulates antimicrobial peptide expression by both glucocorticoid and β-adrenergic mechanisms

Eur J Dermatol. 2011 May;21 Suppl 2:48-51. doi: 10.1684/ejd.2011.1273.


Psychological stress (PS) exerts well-known negative consequences for permeability barrier function in humans and mice, and deterioration of barrier function appears to be attributable largely to excess production of endogenous glucocorticoids (GC). More recently, PS has been shown to compromise antimicrobial defense, also by GC-dependent mechanisms. We assessed here changes in a third antimicrobial peptide (AMP); i.e., the neuropeptide, catestatin (Cst), which also is expressed in the outer epidermis, and previously shown to be regulated by changes in permeability barrier status. In these studies, PS again provoked a decline in both mouse cathelicidin (CAMP) and mouse β-defensin 3 (mBD3) expression, in a GC-dependent fashion. In contrast, Cst immunostaining instead increased after short-term PS, but then began to decline with more sustained PS. In cultured keratinocytes, we showed further that GC downregulate Cst expression, but β-adrenergic blockade increased immunostaining for Cst in the face of long-term PS. Furthermore, β-adrenergic blockade also upregulated CAMP and mBD3 expression. Together, these results suggest that both endogenous GC and β-adrenergic signaling regulate AMP expression.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Animals
  • Antimicrobial Cationic Peptides / metabolism*
  • Chromogranin A / metabolism*
  • Female
  • Keratinocytes / metabolism
  • Mice
  • Peptide Fragments / metabolism*
  • Skin Diseases, Infectious / metabolism
  • Stress, Psychological / metabolism
  • Stress, Psychological / physiopathology*
  • beta-Defensins / metabolism


  • Antimicrobial Cationic Peptides
  • Chromogranin A
  • Peptide Fragments
  • beta-Defensins
  • chromogranin A (344-364)