2026-06-14T13:46:06Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/93312024-11-29T15:45:21Zcom_20.500.12105_2173com_20.500.12105_2051col_20.500.12105_19597
Repisalud
author
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
funder
Ministerio de Economía y Competitividad (España)
funder
Unión Europea. Comisión Europea. European Research Council (ERC)
2020-03-25T14:28:18Z
2020-03-25T14:28:18Z
2019-10-22
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
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.
eng
AP-1
JunB
Atopic dermatitis
Dysbiosis
Microbiota
Skin inflammation
Type 2 immunity
Cutaneous Immune Cell-Microbiota Interactions Are Controlled by Epidermal JunB/AP-1
journal article
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CutaneousImmuneCell-Microbiota_2019.pdf.txt
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