JEADV: Microbial dysbiosis in a mouse model of atopic dermatitis mimicking changes in the human microbiota

The skin is our largest organ, besides regulating body temperature and moisture, it also protects us from different environmental factors and is the first barrier against harmful microorganisms, toxins or other potentially harmful substances
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The skin has its own composition of microbiota, which together with skin cells and the immune system act as a functional unit of barrier defense

Under healthy conditions, the human skin microbiota is mainly composed of bacteria and actinomycetes such as Staphylococcus, Propionibacterium and Corynebacterium
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Disruption of the balanced skin microbiota is often associated with skin diseases such as atopic dermatitis (AD), in which Staphylococcus aureus and other pathogenic microorganisms colonize the skin and are prevalent in healthy skin flora

The skin microbiota is mainly composed of bacteria and actinomycetes such as Staphylococcus, Propionibacterium and Corynebacterium

Topical application of calcipotriol or oxazolone induced AD in mice
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Following induction of AD-like dermatitis, including IgE induction, skin microbial communities were profiled and compared to human AD

We detected key differences in the microflora composition of diseased skin
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Compared with calcipotriol treatment, application of oxazolone resulted in significant changes in the skin microflora and a dramatic decrease in bacterial richness

Figure 1 Phenotypic characterization of two AD mouse models
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(A) Experimental setup: calcitriol (red) and oxazolone (green)

Figure 1 Phenotypic characterization of two AD mouse models

Source: Amar Y, Schneider E, Köberle M, Microbial dysbiosis in a mouse model of atopic dermatitis mimics shifts in human microbiome and correlates with the key pro-inflammatory cytokines IL-4, IL-33 and TSLP.

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