Atopic dermatitis (AD) is a skin condition that has origins in early childhood. This article explores the groundbreaking work of Dr. Alan D. Irvine and his team, who have dedicated years of research to understand the prevalence of AD on the faces of infant’s cheeks provides valuable insights into the early onset of AD, contributing significantly to our understanding of this complex condition.
Skin Maturation in Infants
The team conducted non-invasive skin tests on newborns and continued these tests up to the age of 4 years in various cohorts. This straightforward process enabled the team to examine natural moisturing factors (NMF). Filaggrin, which can be measured using tape strips, accounts for approximately 70% of stratum corneum. The high-performance liquid chromatography (HPLC) method is simple to perform and yields highly reproducible results. The NMF levels in an infant’s cheek are quite low and take longer to mature, reaching maturity around the age of 3 years, unlike the rest of the body which matures much faster. There might be an evolutionary explanation for this, possibly related to the mother’s breast milk or the transfer of antibodies, among other theories.
Introducing Allergens
Infant skin has low cohesion, making it easy to strip off, and the corneocytes are notably immature. This becomes a significant factor when food proteins are applied to the cheek rather than consumed orally. Given that infants are not precise eaters, their cheeks can become a potential window of entry for initiation of AD or for allergies. This concept has been seen in a large-scale study in Bristol that examined the use of peanut-containing nipple balm for nursing mothers, which resulted in an increased risk of peanut allergy in their children. The study mentioned above, among others, has shown that oral feeding leading to the exposure of antigens, including food proteins, through the skin can trigger allergies, a characteristic of type 2 immunity. Type 2 immunity is designed to repel parasites and is closely tied to the neural immune axis. For example, the presence of a parasite can cause itching in the nose, leading to sneezing, coughing, vomiting if it is in the gut, or scratching if it is on the skin, all aimed at quickly removing the parasite. This is where Th2 immunity comes into play, linking tightly with the immune system for rapid responses. However, it is not intended to be activated continuously, as is the case with AD.
To conclude, the research conducted by Dr. Alan D. Irvine and his team underscores the intricate nature of AD and its roots in early childhood. The findings highlight the importance of understanding the unique characteristics of infant skin and the role it plays in the onset and progression of AD. This work serves as a reminder of the complex interplay between our external environment and internal biological processes, and the need for continues research in this field of study.
Want to learn more about skin barrier dysfunction in AD? Follow the link to access the full webinar: https://inderostg.wpenginepowered.com/skin-barrier-dysfunction-atopic-dermatitis-and-beyond/
About the Author
Alan D. Irvine, MD, DSc
A key leader in dermatology research, he is a professor of Dermatology at Trinity College in Ireland. Dr. Irvine is the founding president of the Irish Skin Foundation and the International Eczema Council. His research focuses on molecular genetics of skin disease including rare skin disorders.
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