Despite recent advances in understanding microbial diversity in skin homeostasis, the relevance of microbial dysbiosis in inflammatory disease is poorly understood. Here we perform a comparative analysis of skin microbial communities coupled to global patterns of cutaneous gene expression in patients with atopic dermatitis or psoriasis. The skin microbiota is analysed by 16S amplicon or whole genome sequencing and the skin transcriptome by microarrays, followed by integration of the data layers. We find that atopic dermatitis and psoriasis can be classified by distinct microbes, which differ from healthy volunteers microbiome composition. Atopic dermatitis is dominated by a single microbe (Staphylococcus aureus), and associated with a disease relevant host transcriptomic signature enriched for skin barrier function, tryptophan metabolism and immune activation. In contrast, psoriasis is characterized by co-occurring communities of microbes with weak associations with disease related gene expression. Our work provides a basis for biomarker discovery and targeted therapies in skin dysbiosis.
Bibliographical noteFunding Information:
The authors want to thank Prof. A. Andersson (KTH Royal Institute of Technology and Science for Life Laboratory (SciLifeLab)) for providing the 16S primer designs and acknowledge support from SciLifeLab, the national infrastructure SNISS, and Uppmax for assistance in massive parallel sequencing and computational infrastructure. Technical support by D. Lundin, BILS (Bioinformatics Infrastructure for Life Sciences) and T. Keyvanfar is also acknowledged. The research has received funding from the FP7/ 2007–2013 (Grant 261366). The study was partially funded by the Knut and Alice Wallenberg Foundation, the Department of Health via the National Institute for Health Research (NIHR) comprehensive Biomedical Research Centre award to Guy’s & St Thomas’ NHS Foundation Trust in partnership with King’s College London and King’s College Hospital NHS Foundation (guysbrc-2012-1) Trust, and Dunhill Medical Trust, the Association pour la Recherche contre le Cancer (ARC), the European Research Council (Grant IT-DC 281987), Institute National de la Santé et de la Recherche Médicale (BIO2012-02 and BIO2014-08), INCA (2011-1-PL BIO-12-IC-1), Fondation ARSEP (R12023JJ), ANR (ANR-13-BSV1-0024-02, ANR-10-IDEX-0001-02 PSL*, ANR-11-LABX-0043 and ZonMw MKMD grant 114021503) and BIOMAP IMI2 (Grant 821511).
© 2019, The Author(s).