A sympathetic-eosinophil axis orchestrates psychological stress to exacerbate skin inflammation
Summary
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 ato
Content
# A sympathetic-eosinophil axis orchestrates psychological stress to exacerbate skin inflammation
*Published: 2026 Mar 19*
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.
DOI: 10.1126/science.adv5974