Dysbiosis is a hallmark of atopic dermatitis (AD). The composition of skin microbiome communities and the causality of dysbiosis in eczema have not been well established. The objective of this review is to describe the skin microbiome profile in AD and address whether there is a causal relationship between dysbiosis and AD. The protocol is registered in PROSPERO (CRD42016035813). We searched PubMed, Embase, Scopus and ClinicalTrials.gov for primary research studies applying culture-independent analysis on the microbiome on AD skin of humans and animal models. Two authors independently screened the full text of studies for eligibility and assessed risk of bias. Because of heterogeneity no quantitative synthesis was done. Of 5735 texts, 32 met the inclusion criteria (17 published: 11 human and six animal studies). The studies varied in quality and applied different methodology. The skin in AD had low bacterial diversity (lowest at dermatitis-involved sites) and three studies showed depletion of Malassezia spp. and high non-Malassezia fungal diversity. The relative abundance of Staphylococcus aureus and Staphylococcus epidermidis were elevated and other genera were reduced, including Propionibacterium. A mouse study indicated that dysbiosis is a driving factor in eczema pathogenesis. The data are not sufficiently robust for good characterization; however, dysbiosis in AD not only implicates Staphylococcus spp., but also microbes such as Propionibacterium and Malassezia. A causal role of dysbiosis in eczema in mice should encourage future studies to investigate if this also applies to humans. Other important aspects are temporal dynamics and the influence of methodology on microbiome data.

Deficiency of filaggrin appeared to be a driver of increased peripheral levels of Th17 cells. This increase must be acquired as peripheral Th17 cells were found in adult ft/ft mice but not in 2-week-old ft/ft mice indicating involvement of exogenous factors.

Carriers of FLG mutations who have had hand eczema onset in childhood avoid occupational exposure to irritants; the association is most marked with homozygous mutation status combined with atopic dermatitis.

Skin barrier damage after exposure to para-phenylenediamine Stratum corneum Stratum granulosum Stratum spinosum Stratum basale Para-phenylenediamine (PPD) Decreased expression of stratum corneum proteins and genes Disrup on of ght junc ons and decreased expression of ght junc on genes Non-responder hairdresser Allergic contact derma s pa ent Background: p-Phenylenediamine (PPD) is a strong contact allergen used in hair dye that is known to cause allergic contact dermatitis (ACD). Both private and occupational exposure to PPD is frequent, but the effect of PPD exposure in nonallergic occupationally exposed subjects is unknown. Objective: We sought to investigate the effects of PPD exposure on the skin of occupationally exposed subjects with and without clinical symptoms. Methods: Skin biopsy specimens were collected from 4 patients with mild and 5 patients with severe PPD-related ACD and 7 hairdressers without contact dermatitis on day 4 after patch testing with 1% PPD in petrolatum. RNA sequencing and transcriptomics analyses were performed and confirmed by using quantitative RT-PCR. Protein expression was analyzed in skin from 4 hairdressers and 1 patient with ACD by using immunofluorescence staining.