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Nat Commun. 2015 Sep 29;6:8424. doi: 10.1038/ncomms9424.

Antibiotics in neonatal life increase murine susceptibility to experimental psoriasis.

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Mucosal Immunology Section, OPCB, NIDCR, NIH, Bethesda, Maryland 20892, USA.
University of Manchester, Faculty of Life Sciences, Manchester, M13 9PT, UK.
Center of Reproductive Medicine, Shandong Provincial Hospital, Shandong University, Jinan 250001, China.
State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan 610041, China.
The Alkek Center for Metagenomics and Microbiome Research, Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas 77030, USA.
Laboratory of Parasitic Diseases, NIAID, NIH, Bethesda, Maryland 20892, USA.


Psoriasis is an inflammatory skin disease affecting ∼2% of the world's population, but the aetiology remains incompletely understood. Recently, microbiota have been shown to differentially regulate the development of autoimmune diseases, but their influence on psoriasis is incompletely understood. We show here that adult mice treated with antibiotics that target Gram-negative and Gram-positive bacteria develop ameliorated psoriasiform dermatitis induced by imiquimod, with decreased pro-inflammatory IL-17- and IL-22-producing T cells. Surprisingly, mice treated neonatally with these antibiotics develop exacerbated psoriasis induced by imiquimod or recombinant IL-23 injection when challenged as adults, with increased IL-22-producing γδ(+) T cells. 16S rRNA gene compositional analysis reveals that neonatal antibiotic-treatment dysregulates gut and skin microbiota in adults, which is associated with increased susceptibility to experimental psoriasis. This link between neonatal antibiotic-mediated imbalance in microbiota and development of experimental psoriasis provides precedence for further investigation of its specific aetiology as it relates to human psoriasis.

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