The Role of Immune Defects and Colonization of Staphylococcus aureus in the Pathogenesis of Atopic Dermatitis

Atopic dermatitis (AD) is a condition with a complex and not fully understood etiology. In patients with AD, acute skin lesions are colonized by a greater number of Staphylococcus aureus (S. aureus) bacteria than chronic lesions, clinically unchanged atopic skin, or the skin of healthy people. Mechanisms promoting skin colonization by S. aureus include complex interactions among several factors. Apart from increased adhesion of S. aureus in atopic skin, defects of the innate immune response resulting in the lack of restriction of the growth of microorganisms also contribute to susceptibility to colonization by and infection with S. aureus. A deficiency in the endogenous antimicrobial peptides may be partly responsible for the susceptibility to colonization by and skin infection with S. aureus in patients with AD. Majority of isolated S. aureus stains are able to produce exotoxins, which act as superantigens. Moreover, anti-S. aureus-specific IgE was identified and measured in patients with AD, revealing that its level corresponds to the severity of the disease. This review of the literature attempts to identify factors that are involved in the pathogenesis of AD-related S. aureus skin colonization. In the light of presented mechanisms, a reduction of colonization may become both causative and symptomatic treatment in AD.