Dataset Information

Dysbiosis and Staphylococcus aureus Colonization Drives Inflammation in Atopic Dermatitis.

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.

SUBMITTER: Kobayashi T

PROVIDER: S-EPMC4407815 | biostudies-literature | 2015 Apr

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Dysbiosis and Staphylococcus aureus Colonization Drives Inflammation in Atopic Dermatitis.

Kobayashi Tetsuro T Glatz Martin M Horiuchi Keisuke K Kawasaki Hiroshi H Akiyama Haruhiko H Kaplan Daniel H DH Kong Heidi H HH Amagai Masayuki M Nagao Keisuke K

Immunity 20150401 4

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. aureu ...[more]

PMID: 25902485

Similar Datasets

Project description:BackgroundAtopic dermatitis (AD) is the most common inflammatory skin disorder in the general population worldwide, and the majority of patients are colonized with Staphylococcus aureus. Eczema herpeticum is a disseminated herpes simplex virus infection that occurs in a small subset of patients.ObjectivesThe goal was to conduct proteomic profiling of patients with AD based on S. aureus colonization status and history of eczema herpeticum. We hoped to identify new biomarkers for improved diagnosis and prediction of eczema herpeticum and S. aureus susceptibility and to generate new hypotheses regarding disease pathogenesis.MethodsSkin taping was performed on nonlesional skin of nonatopic control subjects and on lesional and nonlesional skin of patients with AD. Subjects were classified according to the history of eczema herpeticum and S. aureus colonization. Proteins were analyzed by using mass spectrometry; diagnostic groups were compared for statistically significant differences in protein expression.ResultsProteins related to the skin barrier (filaggrin-2, corneodesmosin, desmoglein-1, desmocollin-1, and transglutaminase-3) and generation of natural moisturizing factor (arginase-1, caspase-14, and gamma-glutamyl cyclotransferase) were expressed at significantly lower levels in lesional versus nonlesional sites of patients with AD with and without history of eczema herpeticum; epidermal fatty acid-binding protein was expressed at significantly higher levels in patients with methicillin-resistant S. aureus.ConclusionThis noninvasive, semiquantitative profiling method has revealed novel proteins likely involved in the pathogenesis of AD. The lower expression of skin barrier proteins and enzymes involved in the generation of the natural moisturizing factor could further exacerbate barrier defects and perpetuate water loss from the skin. The greater expression of epidermal fatty acid-binding protein, especially in patients colonized with methicillin-resistant S. aureus, might perpetuate the inflammatory response through eicosanoid signaling.

Dataset Information

Dysbiosis and Staphylococcus aureus Colonization Drives Inflammation in Atopic Dermatitis.

Publications

Dysbiosis and Staphylococcus aureus Colonization Drives Inflammation in Atopic Dermatitis.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets