Atopic dermatitis (AD) is a prevalent, persistent, and recurrent inflammatory skin condition with diverse clinical displays and symptom combinations. The underlying processes of AD are intricate and multifaceted. Numerous factors contribute to the development of AD, such as defects in the skin’s structural and immune barriers, imbalances in the skin microbiome, genetic predisposition, and environmental influences. Changes in structural proteins, lipids, proteases, and their inhibitors result in stratum corneum dysfunction, leading to increased skin permeability and transepidermal water loss.
The review published in Frontiers in Molecular Biosciences primarily focuses on the dysfunction of the immune and structural epidermal barriers in AD. It explores the roles of keratinocytes, filaggrin mutations, alterations in lipid content in the stratum corneum, and the impact of the skin microbiome in AD.
Given the growing interest in the skin microbiome’s crucial role in maintaining skin health, substantial efforts have been dedicated to unraveling the intricate interactions between host cells and resident skin microorganisms. Multiple studies over the last decade have demonstrated the close connection between skin immunology and inflammatory processes with the skin’s microbiota. The composition of the microbiota stabilizes during the early years of life, which is unsurprisingly linked to the development of allergic conditions such as food allergies and AD.
Research has indicated that during AD flares, colonization by Staphylococcus aureus increases, while Staphylococcus epidermidis decreases. Conversely, during remission phases, S. epidermidis and species of Streptococcus, Corynebacterium, and Propionibacterium increase. However, it remains unclear whether skin dysbiosis is a symptom or a contributing factor in AD.
The cutaneous microbiome not only plays a crucial role in immune development and regulation but also directly influences epidermal function. In summary, future research should focus on unraveling the complex network of interactions and molecular signaling mechanisms involving keratinocytes, skin immune cells, and microorganisms.
Despite significant advancements in understanding the pathophysiology of AD and its clinical presentations in both adults and children, there are still numerous unanswered questions. These include elucidating the intricate molecular and cellular mechanisms, metabolic aspects, and the specific mechanisms behind alterations in lipid compositions.