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Increase in primary cilia in the epidermis of patients with atopic dermatitis and psoriasis.

Authors :
Rizaldy, Defri
Toriyama, Manami
Kato, Hiroko
Fukui, Runa
Fujita, Fumitaka
Nakamura, Motoki
Okada, Fumihiro
Morita, Akimichi
Ishii, Ken J.
Source :
Experimental Dermatology; Jun2021, Vol. 30 Issue 6, p792-803, 12p
Publication Year :
2021

Abstract

Primary cilia influence cell activity, and thus have a unique role in maintaining cell proliferation and differentiation. In atopic dermatitis (AD) and psoriasis, areas of skin inflammation exhibit dysregulated keratinocyte homeostasis. The role of primary cilia in these conditions remains unclear. The objectives of this study is to elucidate the incidence of primary cilia in skin inflammation and the potential mechanism underlying the dysregulation of keratinocytes. Primary cilia were observed using immunofluorescence staining. Normal skin samples were compared with skin samples from patients with AD or psoriasis in terms of cilia numbers and length. The effect of cytokine stimulation on ciliogenesis in keratinocytes was analysed using a primary keratinocyte culture. IFT88, an important ciliary intraflagellar protein, was blocked in Th2 and Th17 cytokines‐stimulated keratinocytes. These effects were analysed with quantitative polymerase chain reaction and Western blot. Significant increases in ciliated cells were observed in AD and psoriasis skin samples compared with normal skin samples. The stimulation of keratinocytes using Th2 and Th17 cytokines modulated the formation of primary cilia. The amount of IFT88 in the primary cilia associated with the phosphorylation of JNK, but not p38, in keratinocytes stimulated with interleukin‐13, 17A and 22. An increase of ciliated cells in the epidermis may impair keratinocyte differentiation under stress conditions caused by inflammation in both AD and psoriasis patients. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
09066705
Volume :
30
Issue :
6
Database :
Complementary Index
Journal :
Experimental Dermatology
Publication Type :
Academic Journal
Accession number :
150943601
Full Text :
https://doi.org/10.1111/exd.14285