The Role of Immune Defects and Colonization ofStaphylococcus aureusin the Pathogenesis of Atopic Dermatitis

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.

Prevalence of atopy and staphylococcal superantigen‐specific immunoglobulin E (IgE) antibodies and total serum IgE in primary cutaneous T‐ and B‐cell lymphoma

“…In addition to atopic diathesis of the patients, colonization of the skin of SS by SSAg‐producing S. aureus as implied by presence of SSAg‐IgE is an important factor that mediates IgE‐t levels. This has been extensively studied in patients with atopic dermatitis . It would be interesting to learn if IgE‐t levels differ according to SSAg‐producing versus non‐SSAg‐producing strains of S. aureus isolated from the skin.…”

“…This has been extensively studied in patients with atopic dermatitis. 47,48 It would be interesting to learn if IgE-t levels differ according to SSAg-producing versus non-SSAgproducing strains of S. aureus isolated from the skin. Perhaps a difference in the skin microbiome may explain why SSAg-IgE against SEA and SEB are detected twice as often as TSST1 in atopic dermatitis whereas TSST1-IgE was detected more often in our patients with SS.…”

<b><i>Staphylococcus aureus</i></b> and Host Immunity in Recurrent Furunculosis

“…The infection can be particularly fulminant in people infected with human immunodeficiency virus, suffering from diabetes, and in patients undergoing immunosuppressive treatment. Also, in patients with an impaired structure and skin functioning as a barrier which is common in patients with atopic dermatitis, recurrent and severe furuncles are observed [18-20]. Nevertheless, in immunocompetent patients without any history of atopy and metabolic diseases, factors that determine predisposition to the development and recurrence of furuncles are understudied and not fully explained [21].…”

New Cosmetic Formulation for Treatment of Mild to Moderate Infantile Atopic Dermatitis

“…It is remarkable to highlight, defects in skin barrier structure, as well as impairment in functional integrity and reduced ability for self-renewal, seem to play a role in triggering both an immune response and nonspecific inflammatory reaction [2].…”

“…Atopic children show equally important immune deregulation, probably due to a change in the cytokine profile synthetized by Th1 and Th2 subpopulations. A shortage in Th1 subpopulation observed in these patients is associated with reduced secretion of interferon (IFN) gamma which in turn may reduce the activity of natural killer (NK) cells, decrease the number of circulating T lymphocytes and result in an elevated ratio of CD4+/CD8+ lymphocytes [2]. These cells secrete interleukins (IL-4, IL-5 and IL-13) which induce the production of immunoglobulin E (antibody 2 of 9 present in allergies).…”