Antibiotics in neonatal life increase murine susceptibility to experimental psoriasis

Peter Zanvit, Joanne E. Konkel, Xue Jiao, Shimpei Kasagi, Dunfang Zhang, Ruiqing Wu, Cheryl Chia, Nadim J. Ajami, Daniel P. Smith, Joseph F. Petrosino, Brittany Abbatiello, Hiroko Nakatsukasa, Qianming Chen, Yasmine Belkaid, Zi Jiang Chen, Wanjun Chen

研究成果: Article査読

79 被引用数 (Scopus)

抄録

Psoriasis is an inflammatory skin disease affecting a 1/42% of the worlda € 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 I 3I + 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.

本文言語English
論文番号8424
ジャーナルNature communications
6
DOI
出版ステータスPublished - 2015 9 29
外部発表はい

ASJC Scopus subject areas

  • 化学 (全般)
  • 生化学、遺伝学、分子生物学(全般)
  • 物理学および天文学(全般)

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