Scientists have discovered a neuroimmune circuit that links stress to skin inflammation.[5] Specific stress-responsive neural circuits in the brain amplify skin inflammation by influencing immune cells.[5] This mechanism explains how psychological stress aggravates dermatitis.[4][5] The sympathetic-eosinophilic axis drives stress-induced exacerbation of skin inflammation through Pdyn+ neurons.[4] Stress activates the HPA axis, releasing CRH, ACTH and cortisol, which promotes the local production of pro-inflammatory cytokines such as IL-6 and TNF-α in the skin.[1][2] Neurotrophins such as NGF, released under stress by keratinocytes and immune cells, enhance neurogenic inflammation and pruritus.[1] Neuropeptides substance P and CGRP from nerve endings increase vascular permeability and mast cell degranulation, thereby contributing to inflammation.[1][2] These findings offer a mechanistic explanation for the link between stress and skin diseases such as psoriasis or atopic dermatitis.[1][3][5]