Dysbiosis and Staphyloccus aureus Colonization Drives Inflammation in Atopic Dermatitis

Tetsuro Kobayashi, Martin Glatz, Keisuke Horiuchi, Hiroshi Kawasaki, Haruhiko Akiyama, Daniel H. Kaplan, Heidi H. Kong, Masayuki Amagai, Keisuke Nagao

Research output: Contribution to journalArticlepeer-review

198 Scopus citations

Abstract

Staphyloccus aureus skin colonization is universal inatopic 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 Adam17fl/flSox9-Cre mice, generated to model ADAM17-deficiency in human, developed eczematous dermatitis with naturally occurring dysbiosis, similar to that observed inatopic 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 Thelper 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.

Original languageEnglish (US)
Pages (from-to)756-766
Number of pages11
JournalImmunity
Volume42
Issue number4
DOIs
StatePublished - Apr 21 2015

Bibliographical note

Funding Information:
This work was supported by Research for Prevention and Treatment of Immune/Allergic Diseases from the Ministry of Health, Labor and Welfare of Japan, Grant-in-Aid for JSPS Fellows and the US National Institutes of Health (NIH) NCI Intramural Research Programs. We thank Julie A. Segre and Mark C. Udey for helpful discussions and Cynthia Ng, Morgan Park, and Sean Conlan for underlying efforts.

Publisher Copyright:
© 2015 Elsevier Inc.

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