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Sci Rep. 2017 Jul 24;7(1):6348. doi: 10.1038/s41598-017-05740-z.

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

Author information

1
Mucosal Immunology Laboratory, Department of Convergence Medicine, University of Ulsan College of Medicine/Asan Medical Center, Seoul, Korea.
2
ASAN Institute for Life Science, Asan Medical Center, Seoul, Korea.
3
Mucosal Immunology Laboratory, Department of Convergence Medicine, University of Ulsan College of Medicine/Asan Medical Center, Seoul, Korea. mnkweon@amc.seoul.kr.

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.

PMID:
28740238
PMCID:
PMC5524713
DOI:
10.1038/s41598-017-05740-z
[Indexed for MEDLINE]
Free PMC Article

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