Overview
- The Science study links higher self-reported stress to greater eczema severity and elevated eosinophils in blood and skin in a 51-person cohort.
- In mouse models, activating the identified sympathetic neurons worsened dermatitis, while removing either these neurons or eosinophils blocked stress-induced flares.
- Mechanistically, Pdyn+ neurons release CCL11 to engage CCR3 on eosinophils and then signal through beta-2 adrenergic receptors (Adrb2) to activate them.
- Chemical sympathectomy and adrenalectomy experiments indicate peripheral sympathetic nerves, not the hypothalamus–pituitary–adrenal axis, drive the exacerbation.
- Findings suggest stress management and targeting the neuron–eosinophil interface as potential strategies, with experts calling for studies on stress types and relevance to other inflammatory diseases.