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

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

    Research output: Contribution to journalReview articleResearchpeer-review

    17 Citations (Scopus)


    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.
    Original languageEnglish
    Pages (from-to)48-51
    JournalEuropean Journal of Dermatology
    Issue number2 SUPPL
    Publication statusPublished - 1 Dec 2011


    • Antimicrobial peptides
    • Beta-defensin
    • Catestatin
    • Cathelicidin
    • Permeability barrier
    • Psychological stress


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