A neuroimmune circuit links stress to skin inflammation.

Psychological stress exacerbates inflammatory skin diseases, such as atopic dermatitis (1, 2), but the neurobiological mechanisms underpinning this connection are poorly understood. Stress mobilizes two main neuroendocrine systems: the brain (hypothalamus)–pituitary–adrenal gland axis, which leads to the production of cortisol, and the sympathetic nervous system–adrenal gland axis, which triggers the release of catecholamines such as epinephrine and norepinephrine. On page 1269 of this issue, Tian et al. (3) report a previously unrecognized neuroimmune axis that links psychological stress with worsening of atopic dermatitis in mice. The authors identified a population of norepinephrine-producing sympathetic neurons that specifically innervate hairy skin and mediate stress-induced aggravation of skin inflammation in an eosinophil- dependent manner. A better understanding of how the brain communicates with the immune system could open possibilities for targeted therapeutic interventions in stress-related skin disorders. [ABSTRACT FROM AUTHOR]