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- W2736408889 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 markedly expanded Staphylococcus (S.) xylosus in the skin of Nfkbiz -/- mice. Oral administration of antibiotics including cephalexin and enrofloxacin ameliorated skin inflammation. Topical application of S. xylosus also resulted in the expansion of IL-17A-secreting CD4+ T cells along with high levels of pro-inflammatory cytokines and chemokines in the skin of Nfkbiz -/- mice. The expansion of commensal S. xylosus may be one cause of skin dysbiosis in Nfkbiz -/- mice and suggests that the Nfkbiz gene may play a regulatory role in the microbiota-skin immunity axis." @default.
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- W2736408889 date "2017-07-24" @default.
- W2736408889 modified "2023-10-18" @default.
- W2736408889 title "The resident pathobiont Staphylococcus xylosus in Nfkbiz-deficient skin accelerates spontaneous skin inflammation" @default.
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- W2736408889 doi "https://doi.org/10.1038/s41598-017-05740-z" @default.
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