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Background  Psoriasis impacts 1–3% of the world’s population and is characterized by hyper-proliferation of keratinocytes and increased inflammation. At the molecular level, psoriasis is commonly driven by a Th17 response, which serves as a major therapeutic target. Microbiome perturbations have been associated with several immune-mediated diseases such as atopic dermatitis, asthma, and multiple sclerosis. Although a few studies have investigated the association between the skin microbiome and psoriasis, conflicting results have been reported plausibly due to the lack of standardized sampling and profiling protocols, or to inherent microbial variability across human subjects and underpowered studies. To better understand the link between the cutaneous microbiota and psoriasis, we conducted an analysis of skin bacterial communities of 28 psoriasis patients and 26 healthy subjects, sampled at six body sites using a standardized protocol and higher sequencing depth compared to previous studies. Mouse studies were employed to examine dermal microbial-immune interactions of bacterial species identified from our study.    Results  Skin microbiome profiling based on sequencing the 16S rRNA V1–V3 variable region revealed significant differences between the psoriasis-associated and healthy skin microbiota. Comparing the overall community structures, psoriasis-associated microbiota displayed higher diversity and more heterogeneity compared to healthy skin bacterial communities. Specific microbial signatures were associated with psoriatic lesional, psoriatic non-lesional, and healthy skin. Specifically, relative enrichment of  Staphylococcus aureus  was strongly associated with both lesional and non-lesional psoriatic skin. In contrast,  Staphylococcus epidermidis  and  Propionibacterium acnes  were underrepresented in psoriatic lesions compared to healthy skin, especially on the arm, gluteal fold, and trunk. Employing a mouse model to further study the impact of cutaneous  Staphylcoccus  species on the skin T cell differentiation, we found that newborn mice colonized with  Staphylococcus aureus  demonstrated strong Th17 polarization, whereas mice colonized with  Staphylococcus epidermidis  or un-colonized controls showed no such response.    Conclusion  Our results suggest that microbial communities on psoriatic skin is substantially different from those on healthy skin. The psoriatic skin microbiome has increased diversity and reduced stability compared to the healthy skin microbiome. The loss of community stability and decrease in immunoregulatory bacteria such as  Staphylococcus epidermidis  and  Propionibacterium acnes  may lead to higher colonization with pathogens such as  Staphylococcus aureus , which could exacerbate cutaneous inflammation along the Th17 axis.    Electronic supplementary material  The online version of this article (10.1186/s40168-018-0533-1) contains supplementary material, which is available to authorized users.

Alteration of the cutaneous microbiome in psoriasis and potential role in Th17 polarization