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.
Highlights
Atopic dermatitis (AD) is a chronic inflammatory skin disorder characterized by a highly heterogenous clinical picture [1,2]
These processes are mediated by pattern recognition receptors (PRRs) that are stimulated by danger-associated molecular patterns (DAMPs) and pathogen-associated molecular patterns (PAMPs) [62]
The concept was further investigated by Towell et al, who showed that a low concentration of natural moisturizing factor (NMF) resulted in the aberrant expression of corneodesmosin, a target structure bound by fibronectin-binding protein B (FnBPB) and clumping factor B (ClfB) [102]
Summary
Atopic dermatitis (AD) is a chronic inflammatory skin disorder characterized by a highly heterogenous clinical picture [1,2]. AD most commonly manifests as chronic hand eczema, flexural dermatitis, and/or head and neck dermatitis. The predominant manifestations of adult-onset AD included nummular eczema-like and prurigo-like phenotypes, whereas childhood-onset AD was more often characterized by lichenified/exudative flexural dermatitis alone and/or in association with portrait dermatitis. An epidermal barrier defect; Immune dysregulation; Int. J. AD, the epidermal barrier defect and dysregulation of maturation to maintain immune balance within the skin. In AD, the epidermal barrier defect and dysregulation of innate innate and acquired immunity result in the enhanced adhesion and proliferation of some bacterial species, especially and acquired immunity result in the enhanced adhesion and proliferation of some bacterial species, especially staphylococci. Microbial dysbiosis subsequently aggravates the skin defect by degrading the components of the epidermal. Microbial dysbiosis subsequently aggravates the skin defect by degrading the components of the epidermal barrier and barrier and potentiating Th2-skewing. Literature data data suggest suggest that that an an epidermal epidermal barrier barrier defect defect is is the the primary primary factor factor driving driving
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