2026-06-14T06:44:20Zhttps://repisalud.isciii.es/rest/oai/request

oai:repisalud.isciii.es:20.500.12105/93312024-11-29T15:45:21Zcom_20.500.12105_2173com_20.500.12105_2051col_20.500.12105_19597

00925njm 22002777a 4500 dc Uluçkan, Azge author Jimenez Maria, M author Roediger, Ben author Schnabl, Jakob author Díez-Córdova, Lucía T author Troulé, Kevin author Weninger, Wolfgang author Wagner, Erwin Friedrich author 2019-10-22 Atopic dermatitis (AD) is a multi-factorial skin disease with a complex inflammatory signature including type 2 and type 17 activation. Although colonization by S. aureus is common in AD, the mechanisms rendering an organism prone to dysbiosis, and the role of IL-17A in the control of S. aureus-induced skin inflammation, are not well understood. Here, we show several pathological aspects of AD, including type 2/type 17 immune responses, elevated IgE, barrier dysfunction, pruritus, and importantly, spontaneous S. aureus colonization in JunBΔep mice, with a large transcriptomic overlap with AD. Additionally, using Rag1-/- mice, we demonstrate that adaptive immune cells are necessary for protection against S. aureus colonization. Prophylactic antibiotics, but not antibiotics after established dysbiosis, reduce IL-17A expression and skin inflammation, examined using Il17a-eGFP reporter mice. Mechanistically, keratinocytes lacking JunB exhibit higher MyD88 levels in vitro and in vivo, previously shown to regulate S. aureus colonization. In conclusion, our data identify JunB as an upstream regulator of microbiota-immune cell interactions and characterize the IL-17A response upon spontaneous dysbiosis. Cell Rep. 2019 ;29(4):844-859 10.1016/j.celrep.2019.09.042 2211-1247 22111247 Cell reports 31644908 http://hdl.handle.net/20.500.12105/9331 AP-1 JunB Atopic dermatitis Dysbiosis Microbiota Skin inflammation Type 2 immunity Cutaneous Immune Cell-Microbiota Interactions Are Controlled by Epidermal JunB/AP-1