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dc.contributor.author
Zouboulis, Christos C.
dc.contributor.author
Nogueira da Costa, Andre
dc.contributor.author
Makrantonaki, E.
dc.contributor.author
Hou, X.X.
dc.contributor.author
Almansouri, Daifallah
dc.contributor.author
Dudley, J.T.
dc.contributor.author
Edwards, H.
dc.contributor.author
Readhead, B.
dc.contributor.author
Balthasar, O.
dc.contributor.author
Jemec, Gregor B E.
dc.contributor.author
Bonitsis, N.G.
dc.contributor.author
Nikolakis, Georgios
dc.contributor.author
Trebing, Dietrich
dc.contributor.author
Zouboulis, Konstantin C.
dc.contributor.author
Hossini, Amir M.
dc.date.accessioned
2020-03-30T08:36:02Z
dc.date.available
2020-02-12T02:59:42Z
dc.date.available
2020-02-12T08:30:40Z
dc.date.available
2020-03-30T08:36:02Z
dc.date.issued
2020-04
dc.identifier.issn
0926-9959
dc.identifier.issn
1468-3083
dc.identifier.other
10.1111/jdv.16147
en_US
dc.identifier.uri
http://hdl.handle.net/20.500.11850/398607
dc.identifier.doi
10.3929/ethz-b-000398607
dc.description.abstract
Background The large unmet need of hidradenitis suppurativa/acne inversa (HS) therapy requires the elucidation of disease‐driving mechanisms and tissue targeting. Objective Robust characterization of the underlying HS mechanisms and detection of the involved skin compartments. Methods Hidradenitis suppurativa/acne inversa molecular taxonomy and key signalling pathways were studied by whole transcriptome profiling. Dysregulated genes were detected by comparing lesional and non‐lesional skin obtained from female HS patients and matched healthy controls using the Agilent array platform. The differential gene expression was confirmed by quantitative real‐time PCR and targeted protein characterization via immunohistochemistry in another set of female patients. HS‐involved skin compartments were also recognized by immunohistochemistry. Results Alterations to key regulatory pathways involving glucocorticoid receptor, atherosclerosis, HIF1α and IL17A signalling as well as inhibition of matrix metalloproteases were detected. From a functional standpoint, cellular assembly, maintenance and movement, haematological system development and function, immune cell trafficking and antimicrobial response were key processes probably being affected in HS. Sixteen genes were found to characterize HS from a molecular standpoint (DEFB4, MMP1, GJB2, PI3, KRT16, MMP9, SERPINB4, SERPINB3, SPRR3, S100A8, S100A9, S100A12, S100A7A (15), KRT6A, TCN1, TMPRSS11D). Among the proteins strongly expressed in HS, calgranulin‐A, calgranulin‐B and serpin‐B4 were detected in the hair root sheath, koebnerisin and connexin‐32 in stratum granulosum, transcobalamin‐1 in stratum spinosum/hair root sheath, small prolin‐rich protein‐3 in apocrine sweat gland ducts/sebaceous glands‐ducts and matrix metallopeptidase‐9 in resident monocytes. Conclusion Our findings highlight a panel of immune‐related drivers in HS, which influence innate immunity and cell differentiation in follicular and epidermal keratinocytes as well as skin glands.
en_US
dc.format
application/pdf
en_US
dc.language.iso
en
en_US
dc.publisher
Wiley
en_US
dc.rights.uri
http://creativecommons.org/licenses/by-nc-nd/4.0/
dc.title
Alterations in innate immunity and epithelial cell differentiation are the molecular pillars of hidradenitis suppurativa
en_US
dc.type
Journal Article
dc.rights.license
Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
dc.date.published
2019-12-14
ethz.journal.title
Journal of the European Academy of Dermatology & Venereology
ethz.journal.volume
34
en_US
ethz.journal.issue
4
en_US
ethz.journal.abbreviated
JEADV, J. Eur. Acad. Dermatol. Venereol.
ethz.pages.start
846
en_US
ethz.pages.end
861
en_US
ethz.version.deposit
publishedVersion
en_US
ethz.identifier.wos
ethz.identifier.scopus
ethz.publication.place
Oxford
en_US
ethz.publication.status
published
en_US
ethz.date.deposited
2020-02-12T02:59:53Z
ethz.source
WOS
ethz.eth
yes
en_US
ethz.availability
Open access
en_US
ethz.rosetta.installDate
2020-03-30T08:36:15Z
ethz.rosetta.lastUpdated
2021-02-15T09:44:12Z
ethz.rosetta.versionExported
true
ethz.COinS
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