Why do I have atopic dermatits?

Mano con piel agrietada

The prevalence of atopic dermatitis has increased over the past 30 years, to the extent that it is now one of the most common skin diseases worldwide, affecting approximately one fifth of the population in developed countries1. This post will review the basic information you need to know about this disease and the physiological characteristics of atopic skin.

It is important to know that atopic dermatitis does not have a unique cause, in fact, disease progression is triggered by genetic, immune, and environmental factors. To understand the disease, let’s review the basic physiology of healthy skin.

A healthy skin barrier is formed by several layers of cells. The deeper layers contain living cells called keratinocytes that undergo differentiation until becoming dead flattened cells called corneocytes. The differentiation process from keratinocyte to corneocyte requires the involvement of the protein filaggrin, which is important for cell flattening and differentiation2.

The layer of tissue formed by corneocytes is named the stratum corneum and is the uppermost layer of the skin that can be easily seen throughout your body. The structure of the stratum corneum is often referred to as a “brick and mortar” structure, in which bricks represent corneocytes and mortar represents the lipid matrix found between corneocytes. The stratum corneum, as a physical barrier, prevents the body from excessive water loss and protects the skin from external compounds and pathogens3.

Representation of healthy skin (a) and atopic skin barrier (b). Atopic skin has a reduced lipid matrix that allows excessive transepidermal water loss and the entry of pathogens and irritants to the skin. 

The skin barrier in atopic skins has several structural alterations that make them more reactive and vulnerable to external stimuli. These stimuli cause the formation of lesions with sensations of dryness and itching.   

The lipid matrix of a healthy skin contains ceramides, cholesterol, and free fatty acids that support and cover the surface of each corneocyte to form an impermeable barrier. In atopic skin, the levels of free fatty acids and ceramides are decreased causing a greater water loss that leads to a dry skin sensation. Moreover, an altered lipid composition is directly related to an increased risk of bacterial infections4.

On the other hand, mutations in the gene that encodes for filaggrin protein are considered a risk factor to develop atopic dermatitis. Alterations in filaggrin formation and function have been associated with skin barrier impairment due to a potential increase in transepidermal water loss, pH alterations, and dehydration5.

Furthermore, filaggrin is broken down into smaller peptides and free amino acids creating the natural moisturizing factors2,5. These molecules are responsible for maintaining hydration levels and regulating the physiologic pH of the skin.  Healthy skin is known to have a naturally occurring acidic pH, around 5.5, which inhibits skin colonization by pathogenic bacteria such as Staphylococcus aureus. It has been shown that atopic dermatitis patients have significantly elevated skin pH levels, making them more vulnerable to infections4.

All these factors promote the hyperactivation of cutaneous nerve endings that react to environmental circumstances that are not an actual threat. As a result of this activation, the typical uncomfortable sensations of atopic dermatitis such as itching, stinging or irritation occur.

Lastly, atopic dermatitis is characterized by a dysregulated immune response that is related to a skin barrier impairment and the development of lesions. An increased response of Th2 cytokines such asIL-4, IL-13 and, IL-31 has been shown to play an important role in suppression of antimicrobial peptides, increased inflammatory response, sensitivity, and sustained itch in patients with atopic skin4,5.

Considering the multiple factors, the development of atopic dermatitis involves epidermal gene mutations and alterations in the cell-mediated immune response. These factors contribute to skin barrier dysfunction and make the skin more sensible and with a higher inflammatory response upon external factors and pathogens. Therefore, a specific skincare routine for atopic skin is important to maintain skin integrity and prevent atopic dermatitis flare-ups.

Nocisens®, the product range of Prospera Biotech, acts specifically on epidermal neurosensorial receptors, maintaining their activity controlled and helping to soothe the sensations of itching and stinging typical of sensitive and atopic skin.


1. Salvador, S. J., Romero-Perez, D. & Encabo-Duran, B. Atopic Dermatitis in Adults : A Diagnostic Challenge. J. Investig Allergol Clin Immunol 27, 78–88 (2017).

2. Kezic, S. & Jakasa, I. Filaggrin and Skin Barrier Function. Curr Probl Dermatol. 49, 1–7 (2016).

3. Smeden, J. Van & Bouwstra, J. A. Stratum Corneum Lipids : Their Role for the Skin Barrier Function in Healthy Subjects and Atopic Dermatitis Patients. Curr Probl Dermatol. 49, 8–26 (2016).

4. Kim, J. et al. Pathophysiology of atopic dermatitis : Clinical implications. Allergy Asthma Proc. 40, 1–3 (2019).

5. Fortson, E. A., Feldman, S. R. & Strowd, L. C. Management of Atopic Dermatitis. (2017).

Photo by Sharon McCutcheon on Unsplash


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