- Research suggests that chronic stress can trigger eczema flare-ups, a common skin condition characterized by severe itching.
- The mechanisms by which stress causes eczema flare-ups had remained unknown, but now a study by Fudan University in Shanghai, China, has conducted a deep dive into the biological connections.
- It identified a specific network of neurons that, under stress, trigger an immune reaction in the skin that leads to eczema flare-ups.
Atopic dermatitis, also known as eczema, is a skin condition affecting an estimated 16.5 million adults in the United States alone. Around the world, it likely affects as many as 101.27 million adults, if not more.
It often involves persistent itchiness, sometimes severe, the development of roughened, scaly, or discolored skin patches, and scratching too often or too hard can exacerbate symptoms and lead to further skin infections.
There are several ways to manage eczema, including using barrier-repair moisturisers and taking medication such as antihistamines or antibiotics, as prescribed on a case-by-case basis.
However, this skin condition currently has no cure, and its symptoms may come and go, ranging in severity each time.
Resurgences of symptoms are referred to as “flare-ups,” which can cause significant disruptions to daily life and distress, depending on their severity.
Many factors may contribute to flare-ups, but a National Eczema Society survey found that many people living with this skin condition felt that “stress was the single biggest trigger of their eczema flare-ups,” consistent with findings from focus-group-based studies.
A recent study led by researchers from Fudan University in Shanghai, China, delved into the potential mechanisms underlying the link between stress and flare-ups.
The study — whose findings appear in the journal Science — identified a neural network that, when activated by stress, further triggers an immune response that leads to eczema flare-ups.
Speaking to Medical News Today, study co-author Shenbin Liu, PhD, a neurobiologist at Fudan University, said he and his colleagues decided to further probe the relationship between stress and eczema after hearing from dermatologists about the significant impact the condition has on individuals who live with it.
“One aim of our lab is to understand how the brain communicates with peripheral organs. As the body’s primary barrier organ, the skin contains abundant immune cells and nerve fibers and is highly susceptible to influence by our emotions,” said Liu.
“After consulting with dermatologists, we learned that their most severe patients often experience anxiety, sleep loss, and stress-related symptoms. This inspired us to investigate how stress impacts skin inflammation.”
— Shenbin Liu, PhD
Liu and his colleagues recruited 51 participants with a diagnosis of atopic dermatitis for this study, and they used the Perceived Stress Scale (PSS) to measure their stress levels, and the SCORing Atopic Dermatitis (SCORAD) method, and Numeric Rating Scale (NRS) to gauge the severity of skin inflammation.
They also analyzed skin and blood samples from each study participant.
The researchers found that participants who had scored highly on the stress level scale also experienced more severe skin inflammation during eczema flare-ups than those who had scored low stress levels.
Additionally, participants who experienced high stress levels had elevated levels of eosinophils, a type of white blood cell that plays an important role in immune responses.
Using a mouse model of eczema that developed symptoms including skin redness, itchiness, and inflammation, the researchers confirmed that, under stress, these symptoms worsened perceptibly.
When they collected and analyzed skin samples from the mice, the study authors found that samples from animals that had experienced high stress levels contained four times as many eosinophils as those from animals that had not experienced stress.
Next, the research team analyzed nerve cells in the skin and identified a specific group that became activated during psychological stress.
What happened was that these neural cells responded to stress signals from the central nervous system (CNS), which led to the release of certain inflammatory proteins, which, in turn, doubled the level of eosinophils in the skin, leading to inflammation.
Liu illustrated this mechanism by saying that:
“The most remarkable findings of our study reveal that psychological stress communicates with the skin through a specific ‘highway,’ wherein stress activates a distinct subset of skin-innervating sympathetic neurons that not only carry the signal but actively release the chemokine CCL11, which functions as a potent distress beacon to recruit eosinophils, demonstrating that these immune cells serve as the key ‘foot soldiers’ responsible for driving stress-induced exacerbation of atopic dermatitis.”
According to the researcher, “it requires repeated stress challenges” to observe this mechanism in action, suggesting that chronic stress — stress experienced consistently over a long period of time — may be the biggest culprit in eczema flare-ups.
Susan Mayou, MBBS, FRCP, a consultant dermatologist at the Cadogan Clinic in London, United Kingdom, who was not involved in this study, told MNT that “one of [its] most striking findings is the specificity of the pathway involved.”
For Mayou, it was notable that “the study shows that only a particular subset of sympathetic neurons (Pdyn+) drives stress-related inflammation, rather than a broad, generalised stress response,” and that “the traditional stress pathway was not the primary driver” of eczema flare-ups.
“Instead, peripheral nerves played the dominant role. This challenges long-held assumptions about how stress affects inflammatory diseases,” she told us.
“Additionally, the fact that eosinophils alone do not drive eczema, but become highly problematic in the context of stress, helps explain why some immune-targeting treatments have shown inconsistent results in clinical practice,” said Mayou.
Tanya Evans, MD, a board-certified dermatologist and medical director of the Skin Cancer Program at the Melanoma Clinic at MemorialCare Saddleback Medical Center in Laguna Hills, CA, likewise not involved in this study, agreed.
“Previously, stress was thought to worsen eczema through broad systemic pathways like the hypothalamic-pituitary-adrenal (HPA) axis,” Evans explained. This study, she said, challenges that perspective.
Besides the specificity of the pathway involved, she found it surprising that “blocking the adrenal (HPA) pathway worsened inflammation, suggesting it may be protective rather than harmful in this context.”
Like Mayou, she remarked on what she called the “eosinophil paradox,” which appears to explain why certain treatments have failed to effectively treat eczema.
Equally importantly, Evans noted, is that its findings suggest that “stress is not just a trigger — it is biologically wired into the skin’s immune response.”
According to Liu, “the significance of [the current] findings lies in their transformative impact on our understanding of the mind-skin connection, moving the explanation for stress-induced atopic dermatitis flare-ups from a vague psychological concept to a concrete, physical pathway that delineates exactly how a feeling, such as psychological stress, can translate into a biological event, namely inflamed skin, thereby revealing a direct mind-body circuit.”
“Furthermore,” he said, “our work points to a potential new biomarker, as the strong link between stress and elevated eosinophils suggests that clinicians might one day measure a patient’s eosinophil levels not only to assess disease severity but also to gauge the specific contribution of stress to a current flare-up.”
The main goal, however, is to “open the door for novel, targeted therapeutic strategies, including interventions designed to block the stress signal in specific nerves, inhibit the release of the CCL11 chemokine, or prevent eosinophil recruitment and activation,” the researcher emphasized.
Mayou also welcomed the fact that the study “significantly advances our understanding of eczema by identifying a direct biological pathway linking psychological stress to skin inflammation.”
“Importantly,” she said, the research “moves the narrative beyond a vague ‘mind–skin connection’ to a precise neuro-immune mechanism.”
The dermatologist was also hopeful that the newly uncovered evidence might help inform ongoing research on better, “more targeted” eczema treatments.
“I think future research should proceed on multiple fronts, encompassing both translational and basic science investigations,” Liu told MNT. “The most immediate next step would be to verify that the same Pdyn+ sympathetic neuron-CCL11-eosinophil axis operates in human skin.”
“Concurrently, studies should investigate whether stress-induced eosinophilia or elevated CCL11 levels in blood or skin could serve as practical biomarkers to identify patients whose disease is particularly stress-responsive, thereby enabling personalized treatment approaches,” he continued.
Liu also suggested that there may be scope to repurpose existing medications with other indications for the treatment of eczema.
“[R]esearchers should explore whether existing drugs that calm overactive nerves — such as gabapentinoids or local anesthetics — could be reformulated or repurposed to specifically target Pdyn+ sympathetic neurons.”
— Shenbin Liu, PhD
However, the researcher also emphasized that “a deeper understanding of Pdyn+ neurons themselves is also essential” to fully understand the mechanisms involved and identify additional therapeutic pathways.
Are psoriasis and rosacea affected by stress in a similar way?
“The broader relevance of this pathway [involved in eczema activation under stress] also warrants investigation,” added Liu. He wondered: “Does the same mechanism operate in other stress-sensitive dermatological conditions such as psoriasis, rosacea, or urticaria?”
Evans also expressed some curiosity about “whether similar neuroimmune pathways exist in psoriasis, chronic urticaria, [or] prurigo nodularis,” the latter being a condition that often co-occurs with eczema.
Liu finally stressed that the research team’s current findings from experiments in mouse models of eczema should be validated by further research in humans, a point also made by both Evans and Mayou.
“The key next step is translating these findings from animal models into human clinical studies. We need to confirm whether this same neuro-immune pathway operates in patients with eczema and how strongly it influences disease severity,” Mayou told us.
“Equally important is integrating psychological interventions into treatment models. Future research should investigate whether stress-reduction strategies, such as cognitive behavioural therapy, mindfulness or sleep optimisation, can measurably reduce inflammation via this pathway.”
— Susan Mayou, MBBS, FRCP
For now, people living with eczema must continue to explore the treatment avenues that work best for them on an individual basis, with the help of their trusted medical professionals.
Reflecting on lessons from the current study, Mayou said the conclusion “reinforces the importance of managing both the skin and the nervous system” in this skin condition.
According to her, some practical strategies aligned with this approach include:
- prioritizing skin barrier repair through the regular use of emollient creams, and by avoiding harsh soaps, which “helps reduce baseline inflammation and vulnerability to flare-ups,”
- identifying and minimising eczema triggers, which can include “common factors such as allergens, temperature changes, and [skin] irritants,”
- taking a proactive attitude to stress management, where “techniques such as mindfulness, breathing exercises, and improving sleep quality can help reduce flare frequency,”
- breaking “the itch–scratch cycle” by taking easy steps, such as “keeping nails short, using anti-itch treatments, and applying cold compresses,”
- and finally, seeking early treatment for symptoms, as “prompt use of prescribed topical therapies during early flare signs can prevent escalation.”
“Ultimately, eczema management should be holistic, addressing both physical and psychological drivers, as they are more interconnected than previously understood,” Mayou concluded, and Evans agreed.
“This study reinforces a multidimensional approach, not just skin-directed therapy,” said Evans, who also stressed that dermatologists have a duty to “help patients understand [that] your eczema is not just skin-deep — your nervous system and immune system are working together.”
