Category: Dermatology

Categories : Dermatology Immune SystemTags :

New Study Identifies a Key Protein’s Role in Psoriasis

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A new study on psoriasis has determined that a protein called NF-kB c-Rel can intensify the condition’s symptoms when activated by signals from the body’s immune system. Understanding how “c-Rel” affects skin inflammation could lead to new treatments, said the researchers at Case Western Reserve University School of Medicine.

The study, published recently in eBioMedicine, examined how c-Rel contributes to the function of dendritic cells (DCs), a type of immune cell. The study examined how c-Rel responds to specific immunological signals through Toll Like Receptor 7 (TLR7), which regulates innate immunity and inflammation, exacerbating psoriasis.

The researchers also found the absence of c-Rel alleviates inflammation that causes red, scaly patches on the skin. TLR7 meanwhile is known to be activated by diseases such as HIV and HPV, which are also linked to the development psoriasis.

“We believe that by focusing on c-Rel and TLR7, scientists might be able to create more targeted treatments that reduce inflammation and help psoriasis symptoms,” said Parameswaran Ramakrishnan, associate professor of pathology, member of the Case Comprehensive Cancer Center and researcher at Louis Stokes Cleveland VA Medical Center, the study’s principal investigator.

“This may help relieve the discomfort millions of people live with skin inflammation.”

The researchers examined skin samples from psoriasis patients and a mouse model with similar skin changes.

They analysed c-Rel levels and its behaviour in specially engineered cells lacking the protein; they also examined the mouse model lacking c-Rel.

Their goal: to better understand how c-Rel impacts the immune response in psoriasis.

“Our research shows that c-Rel plays a major role in psoriasis inflammation,” said Angela Liu, lead author and a recent graduate of the School of Medicine’s pathology department.

“We saw higher levels of c-Rel in psoriasis; mice lacking c-Rel were significantly protected from developing psoriasis and showed less inflammation.”

Ramakrishnan said their study revealed the potential role for TLR7 and c-Rel signalling in human psoriasis. A range of viruses that activates TLR7, including human immunodeficiency virus (HIV), human papilloma virus (HPV) and hepatitis C virus (HCV), are linked to the development of psoriasis.

“The research warrants future studies on TLR7-c-Rel-dependent molecular mechanism regulating DC function as a potential link for how viral TLR7 activation is involved in worsening psoriatic disease,” Ramakrishnan said. “From a broad perspective, it would be interesting to further explore the role of c-Rel and TLR7 in other biologically relevant diseases involving these proteins, such as systemic lupus erythematosus and wound-healing in diabetes.”

Source: Case Western Reserve University

Categories : Cancer DermatologyTags :

Reaffirming Commitment to the Fight Against Cancer This World Cancer Day

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4 February 2025 – As the world unites to mark World Cancer Day, L’Oréal South Africa reaffirms its unwavering commitment to supporting individuals affected by cancer through groundbreaking initiatives in research, patient care, and workplace inclusion. Over the past three years, efforts have been strengthened through a series of global and local programmes designed to ease the journey of cancer patients and survivors while advancing scientific innovation in supportive care.

The L’Oréal Dermatological Beauty team leads this commitment with two major initiatives. Save Your Skin focuses on skin cancer prevention and early detection, promoting safe sun habits and strong photoprotection. Fight with Care addresses the dermatological side effects experienced by over 80% of cancer patients undergoing treatment, advancing scientific research in supportive care, training healthcare professionals, and providing direct support through educational resources and partnerships with 50 NGOs worldwide, including the Union for International Cancer Control (UICC) and the Multinational Association of Supportive Care in Cancer (MASCC).

Recognising the profound impact of cancer on employees and their families, the Share & Care programme, now in its tenth year, has been expanded to provide financial assistance to employees diagnosed with cancer, psychological and emotional support services, and practical aid to ease their journey through treatment and workplace reintegration. This programme aligns with our leadership in the Working with Cancer charter, advocating for workplace inclusion, care, and long-term support.

Believing in the transformative power of beauty, L’Oréal has introduced dedicated wellness therapy programmes in hospitals and specialised care centres. These include skincare treatments to alleviate the side effects of cancer therapies, beauty services such as make-up sessions to restore confidence and enhance well-being, and therapeutic massages and wellness sessions to improve overall quality of life.

In South Africa, L’Oréal has partnered with the Look Good, Feel Better campaign for over 20 years. This initiative has been a beacon of hope for women undergoing cancer treatment, providing beauty workshops designed to help them regain confidence and a sense of normality during their journey. By offering expert guidance on skincare, make-up, and emotional well-being, the programme empowers participants to face their treatment with renewed strength.

As part of ongoing efforts to support underserved communities, L’Oréal is introducing the Healing Pouch initiative, which donates full-size oncology skincare essentials—including cleansers, emollients, sun care, and wound creams, to hospitals, NGOs, and patient associations. These products, specifically formulated for sensitive and oncology-affected skin, provide essential relief while reinforcing the belief that touch, and tenderness are powerful agents of healing.

“As we mark World Cancer Day, we stand in solidarity with cancer patients, survivors, healthcare professionals, and our own employees,” said Thandi Kunene, Corporate Affairs Lead at L’Oréal South Africa. “Through continued investment in research, support programmes, and longstanding partnerships such as Look Good, Feel Better, we remain steadfast in our mission to make a meaningful difference in the lives of those affected by cancer.”

Through these global and local initiatives, L’Oréal remains committed to advancing cancer awareness, fostering inclusion, and delivering tangible support, because care is at the heart of everything we do.

Categories : Dermatology Immune SystemTags :

Topical Mupirocin Reduces Cutaneous Lupus Inflammation

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A woman with Systemic Lupus Erythematosus. Source: Wikimedia CC0

Researchers have found that topical mupirocin is effective in reducing rashes caused by systemic lupus erythematosus. Instead of directly lowering inflammation, the treatment kills bacteria that promote it. The findings are published in Arthritis & Rheumatology.

Cutaneous lupus erythematosus is a common manifestation of systemic lupus erythematosus, caused by the autoimmune conditions. The condition is characterised by rashes on various parts of the body including the face and scalp, hair loss and scarring of the skin.

The standard treatment for cutaneous lupus erythematosus is using immunosuppressants and biologic drugs to reduce inflammation. While the medications can be helpful, many patients with systemic lupus erythematosus already take several drugs and are looking for alternatives to pills.

J. Michelle Kahlenberg, MD, PhD, a professor of internal medicine in the Division of Rheumatology at University of Michigan Health led a team of researchers investigating topical mupirocin which is one such alternatives.

This trial was based on Kahlenberg’s previous discovery that cutaneous lupus rashes are often colonised with a common skin bacteria, Staphyloccous areus, also known as staph, and contributes to inflammation in the rashes. Mupirocin kills this type of bacteria.

The study randomly selected systemic lupus erythematosus patients currently experiencing cutaneous lupus erythematosus flares to treat their skin lesions with mupirocin or with an inactive control, petrolatum jelly.

Samples from the nose and lesional skin were used to determine baseline and post treatment Staphylococcus abundance and microbial community profiles. Paired samples collected prior to treatment with the topical solution and seven days after treatment showed decreases in lesional staphylococcus aureus in the mupirocin treated samples.

Importantly, the reduction in staph also was accompanied by a reduction in inflammatory signals, including interferon-driven gene expression, in the lesions.

“In addition to decreasing the inflammation by decreasing lesional staphylococcus aureus, the mupirocin treatment also lowered skin monocyte levels, which are important in driving cutaneous lupus,” said Kahlenberg.

Mupirocin is a prescription treatment, and while this early study showed signs of decreasing inflammation, the study wasn’t designed to see if it can decrease the rash of cutaneous lupus erythematosus.

“Additional larger studies are needed to determine whether topical antibiotics will be helpful to make rashes go away,” Kahlenberg said.

“However, this is an exciting first step to show that there may be additional treatments that can improve inflammation beyond our usual immunosuppressant and biologic drugs.”

Source: Michigan Medicine – University of Michigan

Categories : Dermatology New Compounds and TreatmentsTags :

Microbial Therapy Offers New Hope for Vitiligo Patients

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A natural compound derived from gut-friendly bacteria significantly slows the progression of vitiligo and may restore pigmentation, reports a new Northwestern University pre-clinical study in mice. 

The findings, published in the Journal of Investigative Dermatology, could offer hope to millions affected by the autoimmune disease, which causes visible patches of skin discoloration and carries profound emotional and physical consequences.

“The results in our model were astonishing,” said senior study author I. Caroline Le Poole, a professor of dermatology and microbiology-immunology at Northwestern University Feinberg School of Medicine. 

“We found that administering a microbial compound weekly to vitiligo-prone mice significantly suppressed disease progression. It made a spectacular difference in an aggressive model of the disease.”

What is vitiligo?

Vitiligo affects 0.5% to 2% of the global population and is linked to other health challenges, including higher risks of cardiovascular disease, psychological distress and endocrine disorders.

Discoloration often appears on the face, scalp, hands and arms, as well as around body openings like the mouth and genitals. Many individuals with vitiligo also have at least one other autoimmune condition.

How the study was conducted

Le Poole and her colleagues administered a microbial product weekly to vitiligo-prone mice over an 18-week period. By the end, pigment loss on the mice’s backs was reduced by 74%.

The product reduced killer T cells that attack the skin’s pigment and increased protective regulatory T cells, which are typically scarce in vitiligo patients.

“This simple microbial compound could work as a standalone therapy, or in synergy with existing treatments,” Le Poole said.

Existing therapy has limitations

In 2022, the FDA approved the first re-pigmentation therapy for vitiligo: Opzelura (ruxolitinib) cream. Clinical trials found that only 30% of patients using the cream regained 75% or more skin re-pigmentation on the face.

“Our findings about the effectiveness of microbial therapy could give hope to patients who are not well-served by existing treatments,” Le Poole said.

Vitiligo is more severe in patients with darker skin

Le Poole, who has spent more than 30 years studying vitiligo, said the disease has been found to be more severe in people with darker skin tones. The visibility of the discolouration in people with darker skin can also amplify stigma and emotional distress. 

“Patients often feel powerless as they watch their disease progress, unsure how they will look next month,” Le Poole said. “For many, stabilising the disease would be life changing.” 

While the disease can affect self-esteem – particularly for adolescents navigating social pressures – some people embrace it.

“We’ve seen beautiful models with vitiligo challenging societal norms, and that’s wonderful,” Le Poole added. “But for those who want treatment, it’s important to provide real options that can halt disease progression.”

Next steps

The next challenge is adapting the microbial product for human use. “Weekly injections could work, but we need to explore simpler options, like a food additive or ointment,” said Le Poole. “We also need to understand how long the effects last and the best timing for treatment.”

Le Poole added that the same microbial compound she and her colleagues injected in mice could potentially treat other autoimmune conditions, particularly those involving killer T cells in the skin.  

“Our next step is collaborating with scientists from several institutions to refine the compound, understand its mechanisms and determine whether it works alongside existing treatments for auto-immune disease.”

Source: Northwestern University

Categories : Cancer DermatologyTags :

New Viral Treatment for Basal Cell Carcinoma Shines in Trials

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Dermoscopy of an approximately 16mm nodular basal cell carcinoma showing telangiectatic vessels. Source: Wikimedia CC4.0

Basal cell carcinomas, the most common form of skin cancer, occur in chronically sun-exposed areas such as the face.  Locally advanced tumours in particular can be difficult to treat surgically. A research team from MedUni Vienna and University Hospital Vienna has now investigated the effectiveness of a new type of therapy and achieved promising results: The active substance TVEC led to a reduction in the size of the basal cell carcinoma in all study participants, which not only improved surgical removal, but also led to a complete regression of the tumour in some of the patients. The study was published in the top journal Nature Cancer.

In the study Talimogene Laherparepvec (TVEC) was used, which has so far only been approved for the treatment of superficial melanoma metastases. TVEC is a genetically modified herpes simplex virus that specifically destroys tumour cells and simultaneously activates the immune system. The aim of the study was to reduce the size of the tumour before a planned operation so that patients would not suffer any functional or cosmetic restrictions after the procedure. The study included 18 patients who would have required a flap or skin graft due to the size and localisation of their basal cell carcinoma. They each received six intralesional injections of TVEC over a period of 13 weeks before the tumour was surgically removed.

“This enabled the tumour to be reduced in size in half of the patients to such an extent that surgery with direct wound closure was possible. In a third of the cases, the subsequent histological examination even showed no more living tumour cells. All treated tumours at least became smaller, and no tumour grew further under the therapy. The treatment was well tolerated by the patients,” says the principal investigator Christoph Höller, Head of the Skin Tumour Centre at the Department of Dermatology, summarising the results. “The new treatment option for basal cell carcinoma can not only simplify surgery, but also help to avoid disfiguring operations and functional limitations,” adds first author Julia Ressler, also from the Department of Dermatology. In addition to the clinical studies, the researchers from the Department of Dermatology, in cooperation with the St. Anna Children’s Hospital, carried out comprehensive analyses that show that the immune defence in the tumour tissue is strengthened in the course of therapy with TVEC.  

These results suggest that TVEC could be a promising option for the neoadjuvant, i.e. pre-surgical, treatment of basal cell carcinoma, particularly in patients for whom major surgery should be avoided. Further studies are to follow in order to confirm the benefits of this new option in a larger patient population.

Source: Medical University of Vienna

Categories : Dermatology GastrointestinalTags :

Inflammation may Explain the Prevalence of IBD in Psoriasis Sufferers

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Irritable bowel syndrome. Credit: Scientific Animations CC4.0

People with psoriasis often have invisible inflammation in the small intestine with an increased propensity for ‘leaky gut’, according to new research at Uppsala University. These changes in the gut could explain why psoriasis sufferers often have gastrointestinal problems and are more prone to developing Crohn’s disease. The study is published in Biochimica et Biophysica Acta (BBA) – Molecular Basis of Disease.

Psoriasis is a hereditary, chronic skin condition that can also result in inflammation of the joints. Chronic inflammatory bowel diseases (IBD), especially Crohn’s disease, are more common in patients with psoriasis than in the rest of the population.

“Previous research has also shown that people with psoriasis have more gastrointestinal problems than the general population. However we didn’t know much about why this is the case. With our study, we can now show that people with psoriasis often have invisible inflammation in their small intestines, with an increased risk of what’s called leaky gut,” says Maria Lampinen, researcher at Uppsala University.

Pro-inflammatory activity in the gut

The study involved 18 patients with psoriasis and 15 healthy controls as subjects. None of the participants had been diagnosed with gastrointestinal diseases. Samples were taken from both their small and large bowel. The researchers then studied different types of immune cells in the mucous membrane.

“It turned out that psoriasis sufferers had higher numbers of certain types of immune cells in their small intestine, and the cells showed signs of pro-inflammatory activity. Interestingly, we found the same type of immune cells in skin flare-ups from psoriasis patients, suggesting that the inflammation of the skin may have an impact on the gut, or vice versa.

Increased propensity for leaky gut

Normally, the intestinal mucosa act as a protective barrier that also allows nutrients and water to pass through it. In some autoimmune diseases, the intestinal barrier may function poorly. This is called having a leaky gut, and leads to bacteria and harmful substances leaking through the intestinal barrier and causing inflammation. This can also cause more widespread inflammation when these substances are spread via the bloodstream.

Half of the psoriasis patients in the study had increased intestinal barrier permeability or leaky gut. These same patients also reported more gastrointestinal symptoms such as abdominal pain and bloating than patients with a normal intestinal barrier. They also had elevated levels of inflammatory substances in their intestines.

“Given that the psoriasis patients in our study had relatively mild skin disease and showed no visible intestinal inflammation in a gastroscopy, they had surprisingly clear changes in their small intestine compared to healthy controls. These changes could explain why psoriasis sufferers often have gastrointestinal problems, and an increased risk of developing Crohn’s disease.

Source: Uppsala University

Categories : DermatologyTags :

Survey Sheds Light on the Phenomenon of Topical Steroid Withdrawal

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Painful skin and trouble sleeping are among the problems reported when tapering cortisone cream for atopic eczema, as shown by a study headed by the University of Gothenburg. Many users consider the problems to be caused by cortisone dependence.

Topical steroid withdrawal (TSW) is a phenomenon commonly described as extremely red and painful skin arising when cortisone cream treatment is tapered or stopped.

While TSW is not an established diagnosis, the name indicates that the skin has become dependent on cortisone. Little research has been conducted to identify a dependency mechanism, so scientific support is lacking. At the same time, the term has become commonplace on social media, raising concerns among patients about cortisone cream safety.

Now, a national research group in Sweden, headed by Sahlgrenska Academy at the University of Gothenburg, has conducted the first study in which a larger group has been asked to provide a detailed account of what they consider to be TSW. The results are published in the journal Acta Dermato-Venereologica.

Questionnaire via social media

The study targeted adults with atopic eczema, a group that often uses cortisone cream, who also identified as suffering from TSW. The study was conducted by means of an anonymous questionnaire presented in Swedish in social media forums, with the option to share a link to invite other potential participants. The questionnaire was answered by almost one hundred people aged 18–39, the majority of whom were women.

“We wanted to gain more knowledge about how those who identify as suffering from TSW define the phenomenon and which symptoms they describe,” says Mikael Alsterholm, a researcher at the University of Gothenburg and a senior consultant in dermatology and venereology at Sahlgrenska University Hospital.

The results show variations in how the participants defined TSW. Most common was to define it as a dependence on cortisone, with symptoms arising when tapering or stopping its use, although many others also defined TSW as a reaction to cortisone already during its use.

It was also common to define TSW on the basis of the symptoms seen in the skin, such as redness and pain. While the symptoms described varied, they were largely similar to the symptoms seen in an exacerbation of atopic eczema.

In addition to the skin becoming red, dry, and blistered – mainly on the face, neck, torso, and arms – the participants also described sleep problems due to itching as well as signs of anxiety and depression.

Healthcare and research involvement

A majority of the participants described concurrent symptoms of both atopic eczema and TSW. Cortisone cream was most often cited as the triggering factor, while some cited cortisone tablets and a few cortisone-free treatments.

“It’s important that healthcare professionals and researchers are involved in the discussion on TSW and contribute science-based knowledge where possible. Cortisone cream is an effective and safe treatment for most people, and at present there’s no support for avoiding its use for fear of the types of symptoms described in the context of TSW,” says Mikael Alsterholm.

“At the same time, there’s a patient group with different experiences, expressed as TSW, and their symptoms and the potential causes need to be investigated by means of both research and practical healthcare. To do this, we first need to define TSW. While we understand that this is complicated, we hope that this study can help establish such a definition,” he concludes.

Source: University of Gothenburg

Categories : DermatologyTags :

Sunburn Results from Damage to RNA, not DNA

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The warnings against sunburn are well known: avoid direct sunlight between 12 noon and 3pm, seek out shade and put on sunscreen and a hat. It is also taught that sunburn results from damage to DNA. But that is not the full truth, according the researchers behind a new study conducted at the University of Copenhagen and Nanyang Technological University, Singapore (NTU Singapore).

“Sunburn damages the DNA, leading to cell death and inflammation. So the textbooks say. But in this study we were surprised to learn that this is a result of damage to the RNA, not the DNA that causes the acute effects of sunburn,” says Assistant Professor Anna Constance Vind, who is one of the researchers responsible for the new study.

The study has been published in Molecular Cell.

RNA is a more transient molecule than DNA. A type of RNA, known as messenger RNA (mRNA), functions as the intermediate ‘messenger’ that carries information from DNA to make proteins – the basic building blocks of cellular components.

“DNA damage is serious as the mutations will get passed down to progenies of the cells, RNA damage happens all the time and does not cause permanent mutations. Therefore, we used to believe that the RNA is less important, as long as the DNA is intact. But in fact, damages to the RNA are the first to trigger a response to UV radiation,” Anna Constance Vind explains.

The new study was conducted on mice as well as human skin cells, and the objective was to describe the impact of UV radiation on the skin and what causes these damages. The researchers found the same skin response to UV radiation exists in both mice and human cells.

A built-in surveillance system for RNA damage

mRNA damage triggers a response in ribosomes (protein complexes that “read” the mRNA to synthesise protein), orchestrated by a protein known as ZAK-alpha – the so-called ribotoxic stress response – the new study shows. The response can be described as a surveillance system within the cells, which registers the RNA damage, leading to inflammatory signalling and recruitment of immune cells, which then leads to inflammation of the skin.

“We found that the first thing the cells respond to after being exposed to UV radiation is damage to the RNA, and that this is what triggers cell death and inflammation of the skin. In mice exposed to UV radiation we found responses such as inflammation and cell death, but when we removed the ZAK gene, these responses disappeared, which means that ZAK plays a key role in the skin’s response to UV-induced damage,” says Professor Simon Bekker-Jensen from the Department of Cellular and Molecular Medicine, who is one of the other researchers responsible for the study. He adds:

“So you could say that everything depends on this one response, which monitors all protein translations occurring. The cells respond to the RNA damage, realising that something is wrong, and this is what leads to cell death.”

Faster and more effective response

The result of the study changes our understanding of sunburn and the skin’s defence mechanisms: that RNA damage triggers a faster and more effective response, protecting the skin from further damage.

“The fact that the DNA does not control the skin’s initial response to UV radiation, but that something else does and that it does so more effectively and more quickly, is quite the paradigm shift,” says Anna Constance Vind.

We need to understand the function of RNA damage, as it may in the long term change our entire approach to prevention and treatment of sunburn.

“Many inflammatory skin diseases are worsened by sun exposure. Thus, understanding how our skin responds at the cellular level to UV damage opens the door to innovative treatments for certain chronic skin conditions,” says co-author Dr Franklin Zhong, Nanyang Assistant Professor at NTU’s Lee Kong Chian School of Medicine.

“This new knowledge turns things upside down. I think most people associate sunburn with DNA damage; it is established knowledge. But now we need to rewrite the textbooks, and it will affect future research on the effects of UV radiation on the skin,” Simon Bekker-Jensen concludes.

Source: University of Copenhagen

Categories : DermatologyTags :

A New Insight into the Mechanisms of Epidermal Renewal

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Picture by Macrovector on Freepik

The mechanisms underlying skin renewal are still poorly understood, but interleukin-38 (IL-38), a protein involved in regulating inflammatory responses, could provide insights. Researchers observed it for the first time in the form of condensates in keratinocytes, the cells of the epidermis. The presence of IL-38 in these aggregates is enhanced close to the skin’s surface exposed to atmospheric oxygen. This process could be linked to the initiation of programmed keratinocyte death, a natural process in the epidermis. This study, from University of Geneva (UNIGE) researchers, could bring new perspectives for the study of human epidermis and the illnesses that affect it.

Renewal of the epidermis relies on stem cells located in its lowest layer, which constantly produce new keratinocytes. These new cells are then pushed to the surface, differentiating along the way and accumulating protein condensates. Once they reach the top of the epidermis, they undergo a programmed death, cornification, to create a protective barrier of dead cells.

“The way in which the epidermis constantly renews itself is well documented. However, the mechanisms that drive this process are still not fully understood,” explains Gaby Palmer-Lourenço, associate professor at the Faculty of medicine of UNIGE and principal investigator. The study is published in the journal Cell Reports.

An unexpected role

Interleukin 38 is a small messenger protein that ensures communication between cells. It is known for its role in regulating inflammatory responses and its presence in keratinocytes, the cells of the epidermis, was previously associated with the preservation of the skin’s immune balance. “In keratinocytes in vivo, we found that IL-38 forms condensates, specialized protein aggregates with specific biochemical functions, a behavior that was not known for this protein,” recounts Gaby Palmer-Lourenço. Even more curious, the closer the keratinocytes were to the surface of the skin, the greater the amount of IL-38 within these condensates.

A reaction to oxidative stress

Blood vessels stop in the skin layer located below the epidermis. Therefore, the quantity of oxygen available for the keratinocytes is lower in the basal layers of the epidermis compared to the top layers that are directly exposed to the air that surrounds us. However, even though it is necessary to maintain cell functions, oxygen also causes oxidative stress by forming free radicals, reactive molecules that endanger the cell. “We were able to show that oxidative stress does indeed cause IL-38 condensation under laboratory conditions,” confirms Alejandro Díaz-Barreiro, postdoctoral fellow at the UNIGE Faculty of medicine, and first author of the study.

“Our results lead us to believe that, as we move closer to the epidermal surface, the increasing oxygen concentration promotes the formation of protein condensates, indicating to keratinocytes that they are in the right place to enter cell death,” furthers Gaby Palmer-Lourenço. This hypothesis provides new leads to decipher the mechanisms of epidermal renewal. It could also pave the way for a better understanding of the pathological mechanisms underlying certain skin diseases, such as psoriasis or atopic dermatitis. These questions will be further examined by the research group in future studies.

Contributing to an alternative to animal models

Alejandro Díaz-Barreiro is already working on the next step: “In the model we used previously, the effects of oxidative stress were artificially induced in a single layer of keratinocytes, a scenario that differs from the actual situation in the skin. We are therefore developing a new experimental system to apply oxygen gradients to in vitro reconstituted human epidermis. In this model, only the skin surface will be exposed to ambient air, while the other layers will be protected. This will allow us to study in detail the effect of oxidative stress on epidermal renewal.” By enabling a more precise analysis of human cells, this new system will provide an alternative to animal models often used for the study of skin biology and disease.

Source: Université de Genève

Categories : Dermatology Environmental EffectsTags :

Air Pollution Exposure may be Associated with Eczema

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Data from hundreds of thousands of U.S. adults suggests that each zip code increase of 10 µm/m3 in PM2.5 levels is associated with a doubling in eczema rates among residents

Photo by Kouji Tsuru on Pexels

People living in areas with higher levels of air pollution are more likely to have eczema, according to a new study published November 13, 2024 in the open-access journal PLOS ONE by Dr Jeffrey Cohen of Yale School of Medicine, USA.

The prevalence of eczema has increased globally with industrialisation, suggesting a possible contribution from environmental factors. In the new study, researchers used data from the U.S. National Institutes of Health All of Us Research Program, covering hundreds of thousands of U.S. adults. The current study included 286 862 people for whom there was available demographic, zip code and electronic health record data.

Overall, 12 695 participants (4.4%) were diagnosed with eczema. After controlling for demographics and smoking status, people with eczema were more likely to live in zip codes with high levels of fine particulate matter, or PM2.5, in the air. For every increase of 10 µm/m3 in average PM2.5 air pollution in their zip code, people were more than twice as likely to have eczema.

The authors conclude that increased air pollution, as measured by PM2.5, may influence the risk of developing eczema, likely through its effects on the immune system.

The authors add: “Showing that individuals in the United States who are exposed to particulate matter are more likely to have eczema deepens our understanding of the important health implications of ambient air pollution.”

Provided by PLOS