Category: Dermatology

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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

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Survey Sheds Light on the Phenomenon of Topical Steroid Withdrawal

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Source: Pixabay

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

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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

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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

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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

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Has the Root Cause for Psoriasis Finally been Found?

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Scientists may have uncovered the root cause of psoriasis. New research published in Nature Communications strongly suggests the hormone hepcidin may trigger the onset of the condition. This marks the first time hepcidin has been considered a potential causal factor. In mammals, hepcidin is responsible for regulating iron levels in the body.

Psoriasis is a chronic and sometimes debilitating skin disease affecting 2-3% of the global population. The condition is characterised by red, scaly patches that impact the quality of a patient’s life and can sometimes be life-threatening.

The international research team behind this discovery – which includes Dr Charareh Pourzand at the University of Bath – hopes their finding will lead to the development of new drugs able to block the action of the hormone.

Those most likely to benefit from such a treatment are patients with pustular psoriasis (PP) – a particularly severe and treatment-resistant form of the disease that can affect a patient’s nails and joints as well as skin.

Dr Pourzand, who studies ways to mitigate iron imbalances in the skin, said: “Psoriasis is a life-changing dermatological disease. Patients face a potentially disfiguring and lifelong affliction that profoundly affects their lives, causing them both physical discomfort and emotional distress. The condition can also lead to other serious health conditions.

“A new treatment targeting iron hormone imbalance in the skin offers hope. This innovative approach could significantly enhance the quality of life for millions, restoring their confidence and wellbeing.”

We need skin iron – but not too much

Iron is an essential trace metal, not just for transporting oxygen through the body’s circulatory system but also for maintaining healthy skin: it’s involved in many essential cellular functions, including wound healing, collagen production and immune function. However, iron overload in the skin can be harmful, amplifying the damaging effects of UV sunlight and causing hyperproliferative chronic diseases (where cells grow and multiply more than normal), including psoriasis.

Studies going back 50 years have reported high iron concentrations in the skin cells of psoriatic patients, however the cause of this excess and its significance to the condition have remained unclear until now.

The new study is the first to name hepcidin as the likely link.

Hepcidin is responsible for controlling how much iron is absorbed from food and later released into the body. In healthy individuals, it’s produced exclusively in the liver, however the new study has found that in people with psoriasis, the hormone is also generated in the skin.

Exposure to hepcidin triggers iron overload

In the new study, mice (which have many genetic and physiological similarities to humans) developed a rodent form of psoriasis after being exposed to high levels of skin-produced hepcidin.

This over-abundance of the hormone caused the animals’ skin cells to retain far more iron than was required. In turn, this excess iron triggered both a hyperproliferation of skin cells and an abnormally high concentration of inflammation-inducing neutrophils (a type of immune system cell) in the topmost layer of skin.

These two outcomes – an overproduction of skin cells and an abundance of neutrophils – are main features of human psoriasis.

Psoriasis runs in families though experts believe ‘environmental’ factors such as weight, infections and smoking are also triggers.

A disease with no cure

Currently there is no cure for psoriasis, though treatments that include topical creams, light therapy and oral drugs can help keep symptoms under control for patients with some forms of the condition. Recent treatments have focused on targeting the immune pathways that contribute to psoriasis developing.

Dr Pourzand believes a drug targeting hepcidin has the potential to dramatically improve treatment options for all psoriasis patients.

She said: “Our data strongly suggests hepcidin would be a good target for skin psoriasis treatment. A drug that can control this hormone could be used to treat flare-ups and keep patients in remission to prevent recurrence.

“Also, by adjusting the excess iron in psoriatic skin with customised iron chelators (substances that bind to excess iron in the body and help remove it), we would aim to halt the uncontrolled proliferation of psoriatic skin cells. This hyperproliferation is a major focus of our laboratory’s research on psoriasis therapy, conducted in collaboration with national and international scientists from the Skin@Bath Network, including those from this study.”

Source: University of Bath

Categories : Cancer DermatologyTags :

Common Skin Fungus Malassezia may Invade Tissue, Causing Breast Cancer

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Photo by National Cancer Institute on Unsplash

A common skin fungus, Malassezia globosa may invade deep tissues through the skin or by other means, then cause tumour growth, according to a new study. The study results appear in mBio, an open access journal of the American Society for Microbiology.

“It is important to take care of skin not only for beauty, but also for health,” said corresponding study author Qi-Ming Wang, PhD, a professor in the School of Life Sciences, Institute of Life Sciences and Green Development, Hebei University, Hebei, China. “As a factor promoting tumour growth, intertumoural microorganisms need to be paid more attention.” 

Recently, an increasing number of studies have shown a relationship between fungus and cancer. In the new study, Wang and colleagues subjected mouse breast cancer cells to tumour transplantation and then injected the M. globosa into the mammary gland fat pad. At the end of the experiment, they collected the tumour tissue to measure the tumour size and observe the content of intertumoral M. globosa. The researchers discovered that M. globosa colonises in breast fat pads leading to tumour growth. As a lipophilic yeast, the breast fat pad may provide an external source of lipids for the development of M. globosa, said the researchers. They also found that the pro-inflammatory cytokine interleukin (IL)-17a/macrophage axis plays a key role in mechanisms involved in M. globosa-induced breast cancer acceleration from the tumour immune microenvironment perspective.

“Although still controversial, the relationship between microbes and cancer is gaining attention. The imbalance of the microflora in the tumour may lead to disorder in the tumour microenvironment,” Wang said. “For example, Helicobacter pylori emerged as a potential cause of gastric cancer. In addition, Fusobacterium nucleatum has been identified as a potential colorectal cancer biomarker in stool and is predominantly found in the tumour microenvironment. Bacteria or fungi may play a direct (eg, toxins) or indirect (eg, inhibition of anti-tumoural immune responses) role in the tumorigenesis pathways of many of these risk factors. The imbalance of microbial homeostasis in tumours has a certain significance for cancer diagnosis, treatment and prognosis.” 

According to Wang, although the researchers found that M. globosa can promote the growth of tumours, the related transmission route is still unclear. 

Source: American Society for Microbiology

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Treating Radiation-induced Skin Injuries with Aspirin Hydrogels

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Photo by National Cancer Institute on Unsplash

Radiation is a powerful tool for treating cancer, but prolonged exposure can damage the skin. Radiation-induced skin injuries are painful and increase a person’s chances of infection and long-term inflammation. Now, researchers in ACS Biomaterials Science & Engineering report an aspirin-containing hydrogel that mimics the nutrient-rich fluid between cells and accelerates healing of skin damaged by radiation in animals. With further development, the new salve could provide effective and rapid wound healing for humans. 

Most people undergoing radiotherapy for cancer will experience radiation-induced skin injury that can include redness, pain, ulcers, necrosis and infection. There are few treatments for these wounds, with the most common methods being debridement and hyperbaric oxygenation. Wound dressings made from hydrogels are gaining popularity because they are easy to apply and provide a wet environment for healing that is similar to the inside of the body. Glycopeptide-based hydrogels are especially promising: In laboratory and animal studies, the nanofibre structures have promoted cellular growth and regulated cell adhesion and migration. A research team led by Jiamin Zhang, Wei Wang, Yumin Zhang and Jianfeng Liu proposed loading aspirin, a common anti-inflammatory drug, into a glycopeptide-based hydrogel to create a multifunctional wound dressing for radiation-induced skin injuries.       

In lab tests with cultured cells, the researchers found that the aspirin-contained hydrogel scavenged reactive oxygen species, repaired DNA double-strand breaks and inhibited inflammation caused by radiation exposure without affecting cellular growth. In mouse models of radiation-induced skin injury, the researchers found that dressing wounds for three weeks with the salve reduced acute injuries and accelerated healing – results that the team says point to its potential as an easy-to-administer, on-demand treatment option for reducing radiation damage and promoting healing in humans.

Source: American Chemical Society

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Starvation and Adhesion Drive Formation of Keratinocyte Patterns in Skin

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Skin cell (keratinocyte) This normal human skin cell was treated with a growth factor that triggered the formation of specialised protein structures that enable the cell to move. We depend on cell movement for such basic functions as wound healing and launching an immune response. Credit: Torsten Wittmann, University of California, San Francisco

Fingerprints are one of the best-recognised examples of pattern formation by epithelial cells. The primary cells in the epithelium are the keratinocytes, and they are known to form patterns at the microscopic and macroscopic levels. While factors affecting this pattern formation have been reported, the exact mechanisms underlying the process are still not fully understood.

A team of researchers, led by Associate Professor Ken Natsuga at the Faculty of Medicine, Hokkaido University, have revealed that cell-cell adhesion governs pattern formation in keratinocytes. Their findings were published in the journal Life Science Alliance.

“In this study, we used an immortalised keratinocyte cell line, called HaCaT, which retains all the properties of normal keratinocytes,” Natsuga explained. “In order to ensure that our findings were accurate, we established single-cell cultures from this cell line.”

The team observed pattern formation in both the original heterogeneous cell line, as well as in single-cell-derived cultures. During culturing, the keratinocytes moved randomly and spontaneously formed high- and low-density regions, leading to pattern formation.

The pattern formation was markedly influenced by starvation. When the culture medium was renewed, patterns were obscured, but reappeared as the nutrients in the culture medium were consumed by the keratinocytes.

The team then examined the gene expression in the keratinocytes, which revealed that cell adhesion proteins and keratinocyte differentiation proteins were upregulated in high-density regions. “As cell adhesion is necessary for the development of high-cell-density regions, we specifically investigated the expression of adherens junction (AJ) molecules such as E-cadherin and actin,” Natsuga elaborated. “We found that these molecules were localised at the intercellular junctions of high-density regions.”

The authors then used a mathematical model to confirm that, under spatially uniform density and stress, strong cell adhesion leads to the formation of density patterns. They were also able to demonstrate that the keratinocyte patterns influenced cell proliferation and differentiation, and that serum starvation influences epidermal stratification (a type of differentiation) in skin cells from mice.

“Our study presents a novel and robust model of cell–cell adhesion-induced patterning (CAIP),” concludes Natsuga. “We have deepened our mechanistic insight into cellular organization and its consequences for cell fate decisions and epithelial stratification.”  The team demonstrated that epithelial cell–cell adhesion is essential and sufficient for patterning. Future work will focus on adding more variables to the model to understand other processes that occur concurrently during development.

Source: Hokkaido University

Categories : Dermatology Diet and NutritionTags :

Can Omega-3 Fatty Acid Intake Affect Acne Severity?

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In a study in the Journal of Cosmetic Dermatology that included 60 individuals with mild to moderate acne, following the Mediterranean diet and taking omega-3 fatty acid supplements led to significant reductions in inflammatory and non-inflammatory skin lesions, as well as improved quality of life.

Notably, 98.3% of participants had omega-3 fatty acid deficits at the start of the study. Acne severity lessened significantly in those who reached target omega-3 fatty acid levels during the study.

“Lifestyle interventions, including dietary recommendations, should not be considered in opposition to prescription medications, but rather as a valuable adjunct to any modern acne treatment plan,” said corresponding author Anne Guertler, MD, of the Ludwig Maximilian University of Munich, in Germany. “Future studies should build on the foundation laid by our current findings in a randomised, placebo-controlled design to improve dietary recommendations for acne patients.”

Source: Wiley