| First Author | Kim Y | Year | 2017 |
| Journal | Sci Rep | Volume | 7 |
| Issue | 1 | Pages | 6348 |
| PubMed ID | 28740238 | Mgi Jnum | J:253701 |
| Mgi Id | MGI:5926475 | Doi | 10.1038/s41598-017-05740-z |
| Citation | Kim Y, et al. (2017) The resident pathobiont Staphylococcus xylosus in Nfkbiz-deficient skin accelerates spontaneous skin inflammation. Sci Rep 7(1):6348 |
| abstractText | IkappaBzeta, which is encoded by the Nfkbiz gene, is a member of the nuclear IkappaB family of proteins that act as transcriptional regulators via association with NF-kappaB. 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-gamma-, IL-17A-, and IL-22-secreting CD4+ T cells and of IL-17A-secreting gammadelta+ 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. |
