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 o...

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Autores principales:	Yeji Kim, Yong-Soo Lee, Jin-Young Yang, Su-Hyun Lee, Yun-Yong Park, Mi-Na Kweon
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/029952512e8a468ebc00e61a7f5021d9
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spelling	oai:doaj.org-article:029952512e8a468ebc00e61a7f5021d92021-12-02T12:32:33ZThe resident pathobiont Staphylococcus xylosus in Nfkbiz-deficient skin accelerates spontaneous skin inflammation10.1038/s41598-017-05740-z2045-2322https://doaj.org/article/029952512e8a468ebc00e61a7f5021d92017-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-05740-zhttps://doaj.org/toc/2045-2322Abstract 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.Yeji KimYong-Soo LeeJin-Young YangSu-Hyun LeeYun-Yong ParkMi-Na KweonNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-13 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Yeji Kim Yong-Soo Lee Jin-Young Yang Su-Hyun Lee Yun-Yong Park Mi-Na Kweon The resident pathobiont Staphylococcus xylosus in Nfkbiz-deficient skin accelerates spontaneous skin inflammation
description	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.
format	article
author	Yeji Kim Yong-Soo Lee Jin-Young Yang Su-Hyun Lee Yun-Yong Park Mi-Na Kweon
author_facet	Yeji Kim Yong-Soo Lee Jin-Young Yang Su-Hyun Lee Yun-Yong Park Mi-Na Kweon
author_sort	Yeji Kim
title	The resident pathobiont Staphylococcus xylosus in Nfkbiz-deficient skin accelerates spontaneous skin inflammation
title_short	The resident pathobiont Staphylococcus xylosus in Nfkbiz-deficient skin accelerates spontaneous skin inflammation
title_full	The resident pathobiont Staphylococcus xylosus in Nfkbiz-deficient skin accelerates spontaneous skin inflammation
title_fullStr	The resident pathobiont Staphylococcus xylosus in Nfkbiz-deficient skin accelerates spontaneous skin inflammation
title_full_unstemmed	The resident pathobiont Staphylococcus xylosus in Nfkbiz-deficient skin accelerates spontaneous skin inflammation
title_sort	resident pathobiont staphylococcus xylosus in nfkbiz-deficient skin accelerates spontaneous skin inflammation
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/029952512e8a468ebc00e61a7f5021d9
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The resident pathobiont Staphylococcus xylosus in Nfkbiz-deficient skin accelerates spontaneous skin inflammation

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