title: Transplantation of human skin microbiota in models of atopic dermatitis.
abstract: Atopic dermatitis (AD) is characterized by reduced barrier function, reduced innate immune activation, and susceptibility toStaphylococcus aureus. Host susceptibility factors are suggested by monogenic disorders associated with AD-like phenotypes and can be medically modulated.S. aureuscontributes to AD pathogenesis and can be mitigated by antibiotics and bleach baths. Recent work has revealed that the skin microbiome differs significantly between healthy controls and patients with AD, including decreased Gram-negative bacteria in AD. However, little is known about the potential therapeutic benefit of microbiome modulation. To evaluate whether parameters of AD pathogenesis are altered after exposure to different culturable Gram-negative bacteria (CGN) collected from human skin, CGN were collected from healthy controls and patients with AD. Then, effects on cellular and culture-based models of immune, epithelial, and bacterial function were evaluated. Representative strains were evaluated in the MC903 mouse model of AD. We found that CGN taken from healthy volunteers but not from patients with AD were associated with enhanced barrier function, innate immunity activation, and control ofS. aureus. Treatment with CGN from healthy controls improved outcomes in a mouse model of AD. These findings suggest that a live-biotherapeutic approach may hold promise for treatment of patients with AD.
authors.affiliation: Bacterial Pathogenesis Unit, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, NIH, Maryland, USA.
authors.forename: Ian A
authors.initials: IA
authors.lastname: Myles
authors.affiliation: Bacterial Pathogenesis Unit, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, NIH, Maryland, USA.
authors.forename: Kelli W
authors.initials: KW
authors.lastname: Williams
authors.affiliation: Bacterial Pathogenesis Unit, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, NIH, Maryland, USA.
authors.forename: Jensen D
authors.initials: JD
authors.lastname: Reckhow
authors.affiliation: Bacterial Pathogenesis Unit, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, NIH, Maryland, USA.
authors.forename: Momodou L
authors.initials: ML
authors.lastname: Jammeh
authors.affiliation: Bacterial Pathogenesis Unit, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, NIH, Maryland, USA.
authors.forename: Nathan B
authors.initials: NB
authors.lastname: Pincus
authors.affiliation: Bacterial Pathogenesis Unit, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, NIH, Maryland, USA.
authors.forename: Inka
authors.initials: I
authors.lastname: Sastalla
authors.affiliation: Bacterial Pathogenesis Unit, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, NIH, Maryland, USA.
authors.forename: Danial
authors.initials: D
authors.lastname: Saleem
authors.affiliation: Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, NIH, Maryland, USA.
authors.forename: Kelly D
authors.initials: KD
authors.lastname: Stone
authors.affiliation: Bacterial Pathogenesis Unit, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, NIH, Maryland, USA.
authors.forename: Sandip K
authors.initials: SK
authors.lastname: Datta