ABSTRACT
Dry skin and especially eczematous skin is extremely sensible not only for irritants but also for infections due to a disrupted barrier function. Atopic dry skin shows an enhanced transepidermal water loss (TEWL) denoting an impaired water permeability function and a lowered threshold of irritant responsiveness.1,2 Patients with atopic dermatitis (AD) show a markedly increased rate of colonization or infection with microbial organisms, including Staphylococcus aureus. They act in a bidirectional fashion, both as superantigens and as conventional allergens. Increased numbers of S. aureus are found in over 90% of atopic eczema skin lesions and even in uninvolved skin leading to exacerbation and maintenance of skin inflammation via different mechanisms: exotoxins, enzymes, superantigens, and others.3,4 In contrast, only 5% of healthy subjects harbor this organism. The density of S. aureus on AD lesions has been shown to correlate with cutaneous inflammation and to contribute to the severity of the disease.5,6 Not only bacterial, but also viral and fungal superinfections are well-known risk-factors causing acute and severe disease exacerbation. In patients with psoriasis, only 6.7% suffer from skin infections despite the fact that both skin diseases are characterized by defective skin barriers.7,8 Recently, antimicrobial peptides have been shown to be key elements in the innate immune response system providing the first line of defense in the skin.9 In comparison to psoriasis, AD skin lesions contain significantly lower levels of important antimicrobial molecules, such as defensins and cathelicidins. In detail, low levels of iNOS, IL-8, HBD-2, and the recently identified HBD-3 transcripts count for the failure of patients with AD to mount an adequate host response against a variety of microbes.10,11 Thus, while antimicrobial therapy is an important treatment component in the management of AD, neither an increased skin infection rate nor the need
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Dry Skin and Moisturizers: Chemistry and
for antimicrobials is noted in patients with psoriasis except the use of antibiotics when streptococcal infections precipitate or exacerbate the disease.
