Abstract

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.

Highlights

  • Atopic dermatitis (AD) is a condition with a complex and, up till not fully understood etiology

  • The first reports of the disease date back to ancient times; the first reports in the literature and its presence in medical practice dates back to 1808 when Wilian made his pioneer “clinical” description of prurigo and of a prurigo-like condition with the special emphasis on the itchiness which is a characteristic for atopic dermatitis [1]

  • Heczko et al showed that a shortage of medium-chain-length fatty acids may foster colonization by S. aureus in the epidermis, as they observed an inhibitory effect of the elevated concentration of capric, caprylic, and lauric acid on the growth of S. aureus [23]

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Summary

Introduction

Atopic dermatitis (AD) is a condition with a complex and, up till not fully understood etiology. The first reports of the disease date back to ancient times; the first reports in the literature and its presence in medical practice dates back to 1808 when Wilian made his pioneer “clinical” description of prurigo and of a prurigo-like condition with the special emphasis on the itchiness which is a characteristic for atopic dermatitis [1]. Despite the fact that many descriptions of the symptoms of AD and the causes of their occurrence in the course of the disease exist in the current literature, the entire picture of the disease is not fully elucidated. Itchy skin is the main symptom which appears in every type of AD and forces patients to scratch [9,10,11]

The Role of Epidermal Barrier
Inflammatory Process
Defects of Innate Immune Response
Superantigens
Findings
Therapeutic Implications
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