This month’s continuing education article on page 231 is about the bacteria that make up the ecosystem of the skin. The article describes the various types of bacteria, virus, and fungi, and where they live and what predisposes them to protect or perturbate the protective skin barrier.
As noted in the article, however, there are other mechanisms or lines of defense, including immunologic mechanisms, which protect the skin and serve as an early warning system. Some of our patients bring with them a barrier that is chronically less than prepared to serve its protective function. In this column, I’ll discuss a theoretical framework to stimulate our thinking about the commonalities of what we see, but may not know, or vice versa. The exemplar for this discussion is atopic dermatitis (AD).
Atopic dermatitis is a prototype of alterations in the skin barrier and is a major problem in the patients we see and treat on a daily basis who happen to be at risk for the breakdown of the protective skin barrier. Atopic dermatitis affects 15% to 20% of children1; it is characterized as a complex trait in which genetic factors interact with the external environment to produce a chronicity of inflammation, which can lead to a break in the barrier of the skin. A systematic review estimated the annual direct and indirect costs of AD in the United States at $364 million to $3.8 billion.2 Approximately 10% of individuals from European populations are affected by AD.1–3 Consensus is building that the primary deficit in AD is a “barrier defect.”1
Filaggrin, like other genes, has been recently identified, thanks to the human genome project. Filaggrin or filament-aggregating protein (FLG) is thought to play a role, not only in AD, but in other diseases of the skin. A deficit or mutation of the FLG is thought to be responsible for the atopic triad, often occurring in association with asthma and allergic rhinitis. The FLG mutation carriers manifest a number of entities, including AD (which affects 42% of all mutation carriers), contact allergy, asthma, hay fever, and peanut allergy.2 These genetic variants also influence the severity of asthma and alopecia areata and the susceptibility to herpetic infections as well, all of which we see in our patients.
As it relates to this month’s continuing education topic, “Skin Bacteria: Implications for Wound Care,” AD and its associated manifestations also give rise to the susceptibility to cutaneous bacterial colonization and infection (especially Staphylococcus aureus infection) and an elevation in the pH of the stratum corneum, which may lead to enhanced S aureus adhesion and multiplication.1–3 The exact function of FLG is complex; it is known, however, that its deficiency leads to a failure of the barrier function of the skin. Several serious skin diseases associated with FLG deficiency include ichthyosis vulgaris (characterized by dry scaly skin) and chronic eczema. Filaggrin is a natural moisturizer, containing several hydrophilic amino acids capable of increasing the water-holding capacity of the skin. The FLG discovery has brought about a new field of skin-barrier enhancement therapy (yet to be realized), which represents an exciting opportunity to tackle common diseases.
The exploration of this model allowed us to consider the complexity of the skin barrier and the multifaceted factors that may explain its function. Using the model of FLG to explore deeper functions of the skin barrier enables us to “see what we know.” And finally, a dermatologist should be consulted if your wound patients manifest AD and skin infections that have not been diagnosed.
1. Irvine AD, McLean WI. Breaking the (un)sound barrier: filaggrin is a major gene for atopic dermatitis. J Invest Dermatol 2006; 126: 1200–2.
2. Irvine AD, McLean WI, Leung DY. Filaggrin mutations associated with skin and allergic diseases. N Engl J Med 2011; 365: 1315–27.
3. McGrath JA. Filaggrin and the great epidermal barrier grief. Australas J Dermatol 2008; 49 (2): 67–74.