Department of Dermatology, Hospital del Mar-IMIM, Universitat Autonoma de Barcelona, Barcelona, Spain.
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.
心理压力（PS）对人类和小鼠的通透性屏障功能产生了众所周知的负面影响，而屏障功能的恶化似乎主要归因于内源性糖皮质激素（GC）的过度产生。最近，研究表明 PS 通过 GC 依赖性机制也会损害抗菌防御。在这里，我们评估了第三种抗菌肽（AMP）的变化；即神经肽 catestatin（Cst），它也在外表皮表达，并且先前显示其表达受到通透性屏障状态变化的调节。在这些研究中，PS 再次以 GC 依赖性的方式引发了小鼠抗菌肽（CAMP）和小鼠 β-防御素 3（mBD3）表达的下降。相比之下，短期 PS 后 Cst 免疫染色反而增加，但随着 PS 的持续时间更长，Cst 免疫染色开始下降。在培养的角质形成细胞中，我们进一步表明 GC 下调 Cst 表达，但在长期 PS 时，β-肾上腺素能阻滞剂增加了 Cst 的免疫染色。此外，β-肾上腺素能阻滞剂也上调了 CAMP 和 mBD3 的表达。总之，这些结果表明，内源性 GC 和 β-肾上腺素能信号都调节 AMP 的表达。
