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Immunity. 2015 Apr 21;42(4):756-66. doi: 10.1016/j.immuni.2015.03.014.

Dysbiosis and Staphylococcus aureus Colonization Drives Inflammation in Atopic Dermatitis.

Author information

1
Department of Dermatology, Keio University School of Medicine, Tokyo, Japan, PC160-8582; Dermatology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
2
Dermatology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
3
Department of Orthopedic Surgery, Keio University School of Medicine, Tokyo, Japan, PC160-8582.
4
Department of Dermatology, Keio University School of Medicine, Tokyo, Japan, PC160-8582.
5
Department of Orthopedics, Gifu University, Gifu, Japan, PC 501-1194.
6
Department of Dermatology, Center for Immunology, University of Minnesota, Minneapolis, MN 55414, USA.
7
Department of Dermatology, Keio University School of Medicine, Tokyo, Japan, PC160-8582; Dermatology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: keisuke.nagao@nih.gov.

Abstract

Staphylococcus aureus skin colonization is universal in atopic dermatitis and common in cancer patients treated with epidermal growth factor receptor inhibitors. However, the causal relationship of dysbiosis and eczema has yet to be clarified. Herein, we demonstrate that Adam17(fl/fl)Sox9-(Cre) mice, generated to model ADAM17-deficiency in human, developed eczematous dermatitis with naturally occurring dysbiosis, similar to that observed in atopic dermatitis. Corynebacterium mastitidis, S. aureus, and Corynebacterium bovis sequentially emerged during the onset of eczematous dermatitis, and antibiotics specific for these bacterial species almost completely reversed dysbiosis and eliminated skin inflammation. Whereas S. aureus prominently drove eczema formation, C. bovis induced robust T helper 2 cell responses. Langerhans cells were required for eliciting immune responses against S. aureus inoculation. These results characterize differential contributions of dysbiotic flora during eczema formation, and highlight the microbiota-host immunity axis as a possible target for future therapeutics in eczematous dermatitis.

PMID:
25902485
PMCID:
PMC4407815
DOI:
10.1016/j.immuni.2015.03.014
[Indexed for MEDLINE]
Free PMC Article

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