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A sympathetic-eosinophil neuroimmune axis orchestrates psychological stress to exacerbate skin inflammation

ABSTRACT: Psychological stress is hypothesized to trigger exacerbations of atopic dermatitis (AD). However, the neurobiological mechanisms linking stress to immune processes involved in atopy remain poorly understood. Here, we identified a subtype of skin-specific Prodynorphin (Pdyn)+ noradrenergic sympathetic neurons that closely interact with eosinophils, mediating the stress-induced aggravation of AD. Among AD patients, psychological stress was positively correlated with eosinophilic infiltration and the severity of inflammation. In AD-like murine models, genetic ablation of eosinophils or Pdyn+ sympathetic neurons mitigated stress-induced exacerbation of skin inflammation. Furthermore, optogenetic or chemogenetic activation of Pdyn+ sympathetic neurons precipitated AD inflammation through eosinophils. These neurons promote eosinophil recruitment via the CCL11-CCR3 axis and activate them through the noradrenaline-Adr2 pathway within the inflamed skin. Our findings uncover a neuroimmunological mechanism underlying psychological stress-induced exacerbation of AD, highlighting the Pdyn+ sympathetic-eosinophil axis as a crucial interface between the brain and skin inflammation, with potential therapeutic implications.

ORGANISM(S): Mus musculus

PROVIDER: GSE302016 | GEO | 2026/03/30

REPOSITORIES: GEO

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