The resident pathobiont Staphylococcus xylosus in Nfkbiz-deficient skin accelerates spontaneous skin inflammation.

ABSTRACT: IκBζ, which is encoded by the Nfkbiz gene, is a member of the nuclear IκB family of proteins that act as transcriptional regulators via association with NF-κB. Nfkbiz-deficient (Nfkbiz ^-/-) mice develop spontaneous dermatitis; however, the underlying mechanism has yet to be elucidated. In our study, we found higher skin pathology scores and more serum IgE antibodies and trans-epidermal water loss in Nfkbiz ^-/- than in Nfkbiz-sufficient (Nfkbiz ^+/-) mice. There was also greater expansion of IFN-γ-, IL-17A-, and IL-22-secreting CD4⁺ T cells and of IL-17A-secreting γδ⁺ T cells in the skin of Nfkbiz ^-/- mice than in with Nfkbiz ^+/- mice. Pyrosequencing analysis showed decreased diversity of resident bacteria and marke

SUBMITTER: Kim Y 

PROVIDER: S-EPMC5524713 | biostudies-literature | 2017 Jul

REPOSITORIES: biostudies-literature