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 journalArticle

160 Citations (Scopus)

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 Adam17<sup>fl/fl</sup>Sox9-<sup>Cre</sup> 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
Pages (from-to)756-766
Number of pages11
JournalImmunity
Volume42
Issue number4
DOIs
Publication statusPublished - 2015 Apr 21

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Dysbiosis
Eczema
Atopic Dermatitis
Inflammation
Corynebacterium
Dermatitis
Skin
Langerhans Cells
Microbiota
Epidermal Growth Factor Receptor
Immunity
Anti-Bacterial Agents

ASJC Scopus subject areas

  • Immunology and Allergy
  • Infectious Diseases
  • Immunology

Cite this

Kobayashi, T., Glatz, M., Horiuchi, K., Kawasaki, H., Akiyama, H., Kaplan, D. H., ... Nagao, K. (2015). Dysbiosis and Staphyloccus aureus Colonization Drives Inflammation in Atopic Dermatitis. Immunity, 42(4), 756-766. https://doi.org/10.1016/j.immuni.2015.03.014

Dysbiosis and Staphyloccus aureus Colonization Drives Inflammation in Atopic Dermatitis. / Kobayashi, Tetsuro; Glatz, Martin; Horiuchi, Keisuke; Kawasaki, Hiroshi; Akiyama, Haruhiko; Kaplan, Daniel H.; Kong, Heidi H.; Amagai, Masayuki; Nagao, Keisuke.

In: Immunity, Vol. 42, No. 4, 21.04.2015, p. 756-766.

Research output: Contribution to journalArticle

Kobayashi, T, Glatz, M, Horiuchi, K, Kawasaki, H, Akiyama, H, Kaplan, DH, Kong, HH, Amagai, M & Nagao, K 2015, 'Dysbiosis and Staphyloccus aureus Colonization Drives Inflammation in Atopic Dermatitis', Immunity, vol. 42, no. 4, pp. 756-766. https://doi.org/10.1016/j.immuni.2015.03.014
Kobayashi T, Glatz M, Horiuchi K, Kawasaki H, Akiyama H, Kaplan DH et al. Dysbiosis and Staphyloccus aureus Colonization Drives Inflammation in Atopic Dermatitis. Immunity. 2015 Apr 21;42(4):756-766. https://doi.org/10.1016/j.immuni.2015.03.014
Kobayashi, Tetsuro ; Glatz, Martin ; Horiuchi, Keisuke ; Kawasaki, Hiroshi ; Akiyama, Haruhiko ; Kaplan, Daniel H. ; Kong, Heidi H. ; Amagai, Masayuki ; Nagao, Keisuke. / Dysbiosis and Staphyloccus aureus Colonization Drives Inflammation in Atopic Dermatitis. In: Immunity. 2015 ; Vol. 42, No. 4. pp. 756-766.
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