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

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.