Interactions Between Atopic Dermatitis and Staphylococcus aureus Infection: Clinical Implications

Abstract

Staphylococcus aureus commonly colonizes the skin of atopic dermatitis (AD) patients and contributes to the development and exacerbation of AD. Multiple factors are associated with colonization of AD skin by S. aureus, including the strength of S. aureus-corneocyte adhesion, deficiency of antimicrobial peptides, decreased levels of filaggrin and filaggrin degradation products, overexpressed Th2/Th17 cytokines, microbial dysbiosis and altered lipid profiles. S. aureus colonization on AD skin causes skin barrier dysfunction through virulence factors such as superantigens (toxins), enzymes and other proteins. Furthermore, colonization of AD skin by S. aureus exacerbates AD and may contribute to microbial dysbiosis, allergen sensitization, Th2/Th17 polarization, development of atopic march and food allergy in AD patients. Skin colonization of S. aureus, particularly methicillin-resistant S. aureus (MRSA), is one of the major challenges commonly encountered in the management of AD. Bleach bath, and topical or systemic antibiotics could be used to control S. aureus infection on AD skin. However, careful use of antibiotics is required to control the occurence of MRSA. Recently, various strategies, including microbiome transplant, monoclonal antibodies against virulent toxins, vaccines and recombinant phage endolysin, have been studied to control S. aureus infection on AD skin. Further advances in our understanding of S. aureus could provide us with ways to manage S. aureus colonization more effectively in AD patients.

Keywords: Atopic dermatitis; Staphylococcus aureus; microbiome.

Fig. 1

Staphylococcus aureus colonization on the skin of AD. Multiple factors, including skin barrier dysfunction, deficiency of AMPs, and decreased levels of filaggrin and FDPs, altered skin pH, overexpressed Th2/Th17 cytokines, microbial dysbiosis and altered lipid profiles, contribute to the colonization of S. aureus on AD skin. AD, atopic dermatitis; FDP, filaggrin degradation product; AMP, antimicrobial peptide.

Fig. 2

The pathogenic effects of Staphylococcus aureus on atopic dermatitis. S. aureus expresses superantigens, such as SE and TSST-1, which activate basophils and cause T-cell-mediated inflammation. PSMα and PSMβ families stimulate the release of proinflammatory cytokines from keratinocytes. S. aureus α-toxin and δ-toxin induce keratinocyte cytotoxicity and mast cell degranulation, respectively. Protein A and lipoproteins of S. aureus lead to proinflammatory responses by activating TNFR-1 and TLR2 on keratinocytes, respectively. SE, staphylococcal enterotoxin; TSST-1, toxic shock syndrome toxin-1, DC, dendritic cell; MHC II, major histocompatibility complex class II; TCR, T cell receptor; PSM, phenol-soluble modulins; TNFR-1, tumor necrosis factor receptor-1; TLR2, toll-like receptor 2; TSLP, thymic stromal lymphopoietin; IL, interleukin; KC, keratinocyte.