本篇研究，"A sympathetic-eosinophil axis orchestrates psychological stress to exacerbate skin inflammation"，請見這裡，期刊摘要如下：
Psychological stress is believed to exacerbate dermatitis, yet the neurobiological mechanisms linking stress to immune processes remain elusive.
We identified a subset of prodynorphin-positive (Pdyn+) noradrenergic sympathetic neurons in mice that specifically innervate hairy skin, mediating stress-induced exacerbation of skin inflammation in an eosinophil-dependent manner.
Genetic ablation of Pdyn+ sympathetic neurons or eosinophils mitigated stress-evoked worsening of inflammation in atopic dermatitis–like mice, whereas optogenetic activation of these neurons precipitated inflammation through eosinophils. Pdyn+ sympathetic neurons recruited eosinophils through the CCL11-CCR3 axis and activated them through the adrenergic receptor beta2 (Adrb2) in inflamed skin.
Our findings reveal a neuroimmunological mechanism underlying psychological stress–induced exacerbation of dermatitis, emphasizing the Pdyn+ sympathetic-eosinophil axis as a crucial interface between the brain and skin inflammation, with potential therapeutic implications.
