Cutaneous Immune Cell-Microbiota Interactions Are Controlled by Epidermal JunB/AP-1.

ABSTRACT: Atopic dermatitis (AD) is a multi-factorial skin disease with a complex inflammatory signature including type 2 and type 17 activation. Although colonization by S. aureus is common in AD, the mechanisms rendering an organism prone to dysbiosis, and the role of IL-17A in the control of S. aureus-induced skin inflammation, are not well understood. Here, we show several pathological aspects of AD, including type 2/type 17 immune responses, elevated IgE, barrier dysfunction, pruritus, and importantly, spontaneous S. aureus colonization in JunB^Δep mice, with a large transcriptomic overlap with AD. Additionally, using Rag1^-/- mice, we demonstrate that adaptive immune cells are necessary for protection against S. aureus colonization. Prophylactic antibiotics, but not antibio

SUBMITTER: Uluckan O 

PROVIDER: S-EPMC6856727 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature