The Influence of Microbiome Dysbiosis and Bacterial Biofilms on Epidermal Barrier Function in Atopic Dermatitis—An Update

Abstract

Atopic dermatitis (AD) is a common inflammatory dermatosis affecting up to 30% of children and 10% of adults worldwide. AD is primarily driven by an epidermal barrier defect which triggers immune dysregulation within the skin. According to recent research such phenomena are closely related to the microbial dysbiosis of the skin. There is growing evidence that cutaneous microbiota and bacterial biofilms negatively affect skin barrier function, contributing to the onset and exacerbation of AD. This review summarizes the latest data on the mechanisms leading to microbiome dysbiosis and biofilm formation in AD, and the influence of these phenomena on skin barrier function.

Host-Microbe Interaction on the Skin and Its Role in the Pathogenesis and Treatment of Atopic Dermatitis

“…Microorganisms may be present in a sessile form or form complex multispecies communities within the biofilms. Although reports from the literature show that bacterial biofilms serve as the primary pathogenic factor in a variety of skin diseases, e.g., in acne vulgaris and chronic wounds [33], they are also important to maintain the skin barrier in AD patients.…”

Skin barrier defects in atopic dermatitis: From old idea to new opportunity

“…Another important feature of NL AD skin barrier disruption is the association with microbial dysbiosis and more specifically, S. aureus colonization. 123 , 124 Skin infections are commonly associated with AD flares and treatment of these is important for the management of the disease. 125 As part of the Atopic Dermatitis Research Network, we investigated the phenotype and endotype of AD subjects colonized with S. aureus in a multicenter, cross-sectional study.…”

Cytokine-Mediated Crosstalk Between Keratinocytes and T Cells in Atopic Dermatitis

“…During lesion recovery or treatment of AD flares, skin bacterial diversity is improved and S. aureus proportion is decreased ( 128 , 130 ). Some AD features, such as filaggrin deficiency and altered AMP production, associated with elevated skin pH, may favor S. aureus colonization of lesional skin ( 131 – 135 ). S. aureus can counteract cutaneous antibacterial defense through various AMP resistance mechanisms ( 136 – 138 ) and potentiate skin inflammatory response and barrier dysfunction through secretion of various virulence factors, including superantigens, enterotoxins (SEs), fibronectin-binding protein-1 (FBP1), phenol-soluble modulins (PSMs), α-toxin, and proteases ( 139 ).…”