|Teresa Adamek-Guzik, Tomasz Guzik, Grażyna Czerniawska-Mysik, Juliusz Pryjma |
Atopic dermatitis (AD) is a complex inflammatory disorder of unclear pathogenesis. The major questions are related to the role of environmental allergens as well as to the relevance of intrinsic changes within the immune system underlying AD. Allergic reactivity in AD is driven by imbalance between Thl and Th2 type lymphocytes. The exact role of each subpopulation in the pathogenesis of different phases of AD is discussed. Many studies, however, show that changes in both humoral and cellular immunity in AD patients may facilitate skin colonization and/or infections with Staphylococccus aureus which is present in the lesional skin of majority of patients with AD. It is unclear whether this phenomenon is the origin of observed allergic symptoms or it is secondary to inflammation and skin lesions. The intensity of skin colonization with S. aureus is correlated with the severity of lesions assessed with SCORAD scale. Current evidence suggests that although lesional colonization by S. aureus in AD is secondary to allergic inflammation, the bacteria may significantly exacerbate the lesions state. Staphylococcal cell wall compounds along with enterotoxins may induce inflammatory reactions either directly or as allergens. Levels of anti-staphylococcal enterotoxin s-IgE were demonstrated to correlate with clinical severity of the disease. Determination of the role of bacterial colonization in atopic dermatitis will determine future therapeutic approaches including the application of antibiotics.
In some patients, S. aureus may by eradicated from the skin after standard therapy, and antibiotic administration is therefore not necessery.
Alergia Astma Immunologia, 2001, 6(4), 169-179
keywords: alergia, IgE, bakterie, S. aureus, atopia, allergy, IgE, bacteria, S. aureus, atopy
pages: from 169 to 179
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