- Auteur(s) : Gemma MARTIN-EZQUERRA, Mao-Qiang MAN, Melanie HUPE, Marina RODRIGUEZ-MARTIN, Jong-Kyung YOUM, Carles TRULLAS, Donald S. MACKENZIE, Katherine A. RADEK, Walter M. HOLLERAN, Peter M. ELIAS
, Department of Dermatology, Hospital del Mar-IMIM, Universitat Autonoma de Barcelona, Barcelona, Spain, Dermatology Service, VA Medical Center, 4150 Clement Street, San Francisco, CA; Department of Veterans Affairs Medical Center, and Department of Dermatology, UCSF, San Francisco, CA, USA, Dermatology Service, Hospital Universitario de Canarias, University of La Laguna, Tenerife, Spain, ISDIN, Barcelona, Spain, Department of Surgery, Burn and Shock Trauma Institute, Loyola University Medical Center, Maywood, IL
- Mots-clés : antimicrobial peptides, beta-defensin, cathelicidin, catestatin, permeability barrier, psychological stress
- Page(s) : 48-51
- DOI : 10.1684/ejd.2011.1273
- Année de parution : 2011
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.