Scientists have identified neurons that make disease worse when stressed
By Miriam cleans & Nature magazine
Soothing the skin can help reduce eczema flare-ups.
Ladanifere/iStock via Getty
In people with eczema, stress can trigger flare-ups and make the itching worse. But the link between stress and skin inflammation is unclear.
Now, researchers have identified a network of neurons that respond to stress by activating immune cells in the skin, fueling eczema symptoms.
The results, published in Science now come from a mouse model of atopic dermatitis (AD), a type of chronic eczema that affects more than 200 million people worldwide.
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The study shows “how a feeling, such as psychological stress, can translate into a biological event, namely inflammation of the skin,” says co-author Shenbin Liu, a neurobiologist at Fudan University in Shanghai, China.
Allergic skin diseases, such as Alzheimer’s disease, are caused by overactive immune responses that attack the body’s skin cells. Some people with this condition have a buildup of immune cells called eosinophils in affected skin tissues, which exacerbates the inflammation. But what pushes these cells toward the skin and activates them in AD is unclear.
Itchy cells
In an analysis of skin biopsies and blood samples from 51 people with AD, researchers found that those who reported high levels of stress had more severe skin inflammation and higher eosinophil levels than participants who reported low levels of stress.
To understand what activates this inflammatory signal, the authors created a mouse model of AD with symptoms such as skin redness, itching, and inflammatory responses. When these mice experienced psychological stress, their AD symptoms, such as itching, worsened. The biopsied skin of these stressed animals contained four times more eosinophils than the skin of unstressed controls.
To trace the neural signals linking stress and inflammation, the authors analyzed nerve cells in the skin and identified a group of neurons activated by stress. These cells received signals from the central nervous system involved in stress responses, while producing inflammatory proteins that bring eosinophils to the skin.
Activating these neurons more than doubled the proportion of eosinophils in the skin of AD mice, while blocking them prevented stress from worsening symptoms. According to Liu, the results suggest highly targeted treatments, such as blocking stress-sensitive nerves or the inflammatory molecules they produce.
The work linking stress and eczema “is an important piece of the puzzle,” says Wolfgang Weninger, a clinical dermatologist at the Medical University of Vienna. “But this needs to be translated to humans as the next step.”
This article is reproduced with permission and has been published for the first time March 19, 2026.
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