Eczema and psoriasis are chronic inflammatory skin conditions. While their precise origins are complex, research indicates several interconnected factors contribute to their development and flare-ups. This article explores the key suspected causes, including genetic predispositions, environmental influences, and the roles of the immune system, skin barrier, and microbiome.
Understanding Eczema and Psoriasis
Eczema, often called atopic dermatitis, presents as intensely itchy, dry, and inflamed skin that can appear red, weep, or crust. Psoriasis typically manifests as thick, raised, scaly patches covered with silvery scales, commonly on the elbows, knees, scalp, and lower back. While both involve skin inflammation, their distinct presentations reflect underlying biological differences.
Genetic Predisposition
Genetics play a role in increasing an individual’s susceptibility to both eczema and psoriasis. It is not that genes directly cause these conditions, but rather they can make someone more prone to developing them when other factors are present. For eczema, a frequently identified genetic variation is in the filaggrin (`FLG`) gene, which is involved in maintaining the skin barrier. Mutations in `FLG` can lead to a compromised skin barrier, making individuals more susceptible to eczema, as well as associated allergic conditions like asthma and allergies. Other genes, such as `CARD11` and `KIF3A`, have also been linked to eczema.
For psoriasis, the strongest genetic risk factor identified is `HLA-C06:02`, part of the major histocompatibility complex (`MHC`) genes. These genes are important for the immune system’s ability to distinguish between the body’s own cells and foreign invaders. Mutations in genes like `CARD14` can also contribute to psoriasis. Over 80 susceptibility genes have been identified for psoriasis, highlighting the complex genetic landscape of the condition. Even with a genetic predisposition, developing the condition is not guaranteed, suggesting that other elements contribute to disease onset.
Immune System Dysregulation
Both eczema and psoriasis involve an overactive or misdirected immune system. Normally, the immune system protects the body from harmful invaders, but in these conditions, it mistakenly attacks healthy skin cells or overreacts to benign substances. In eczema, the immune response often involves a Type 2 inflammatory pathway, characterized by allergic inflammation. Specific immune cells and inflammatory signaling molecules, such as interleukins `IL-4` and `IL-13`, promote this allergic response, contributing to inflammation and affecting the skin barrier.
In psoriasis, the immune system’s misdirection primarily involves the Type 17 pathway, which leads to chronic inflammation. Dendritic cells produce interleukins like `IL-23` and `TNF-α`, which in turn activate T helper 17 (Th17) cells. Th17 cells produce large amounts of `IL-17`, `IL-22`, and `IFN-γ`. `IL-17` stimulates the rapid proliferation of skin cells (keratinocytes), leading to the thick, scaly plaques characteristic of psoriasis. This continuous activation creates a cycle of inflammation and skin cell overgrowth.
Environmental Influences and Triggers
External factors can initiate or worsen flare-ups. For eczema, common environmental allergens include dust mites, pollen, pet dander, and certain foods like dairy, peanuts, soy, or wheat. Irritants such as harsh soaps, detergents, fragrances, and certain fabrics like wool can also provoke symptoms. Climate extremes, including dry air, low humidity, or excessive heat and sweating, are triggers. Emotional or chronic stress can also exacerbate eczema, as can exposure to air pollution and tobacco smoke.
Psoriasis flare-ups can be triggered by various environmental factors. Infections, particularly strep throat or other skin infections, are common instigators. Physical injury to the skin, known as the Koebner phenomenon (e.g., cuts, scrapes, sunburns, vaccinations), can lead to new psoriatic lesions. Certain medications, including lithium, some blood pressure drugs, and antimalarial drugs, may also trigger flares. Lifestyle factors like smoking, heavy alcohol consumption, and stress are frequently reported triggers, as are cold and dry weather conditions, while warm and humid conditions may offer some improvement.
The Role of the Skin Barrier and Microbiome
The skin barrier, the outermost layer, protects against external threats and regulates moisture levels. In eczema, a compromised skin barrier, often due to genetic defects in proteins like filaggrin, allows irritants and allergens to penetrate. This permeability leads to water loss, resulting in dry, itchy skin and inflammation. The skin’s microbiome also plays a role. In eczema, an imbalance (dysbiosis) often occurs in the skin microbiome, with `Staphylococcus aureus` becoming dominant during flare-ups. This overgrowth is associated with increased disease severity.
While the link is less direct than in eczema, a disrupted skin barrier can also contribute to psoriasis. In psoriasis, rapid skin cell turnover leads to structural damage and impaired barrier function. This allows irritants to infiltrate, intensifying the inflammation. Changes in lipid composition, such as ceramides, are also observed in the skin barrier in psoriasis. Research explores how alterations in the skin and gut microbiome influence psoriasis. Psoriatic lesions show an increased presence of bacteria like `Streptococcus` and `Staphylococcus`. Imbalances in the gut microbiome can also lead to increased intestinal permeability, potentially triggering systemic inflammation that impacts the skin.