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Aryl Hydrocarbon Receptor Activation Downregulates IL-33 Expression in Keratinocytes via Ovo-Like 1.


ABSTRACT:

Background

IL-33, one of the IL-1 superfamily cytokines, has been shown to be associated with pruritus and inflammation in atopic dermatitis (AD). Furthermore, IL-33 production derived from keratinocytes reportedly has a crucial role in the development of AD; however, the mechanism of IL-33 expression has not been fully understood.

Methods

We analyzed IL-33 expression in normal human epidermal keratinocytes (NHEKs) treated with IL-4.

Results

IL-4 induced the upregulation of IL-33 expression in NHEKs. Based on the findings 1) that ovo-like 1 (OVOL1), a susceptible gene of AD, upregulates filaggrin (FLG) and loricrin (LOR) expression in NHEKs and 2) that reduced expression of FLG and LOR leads to production of IL-1 superfamily cytokines, we examined the involvement of OVOL1 in IL-33 expression in NHEKs. Knockdown of OVOL1 induced upregulation of IL-33 expression. Moreover, because Glyteer, an activator of aryl hydrocarbon receptor (AHR), reportedly upregulates OVOL1 expression, we examined whether treatment with Glyteer inhibited IL-33 expression in NHEKs. Treatment with Glyteer inhibited IL-4-induced upregulation of IL-33 expression, which was canceled by knockdown of either AHR or OVOL1.

Conclusions

Activation of the AHR-OVOL1 axis inhibits IL-4-induced IL-33 expression, which could be beneficial for the treatment of AD.

SUBMITTER: Tsuji G 

PROVIDER: S-EPMC7141508 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature

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Aryl Hydrocarbon Receptor Activation Downregulates IL-33 Expression in Keratinocytes via Ovo-Like 1.

Tsuji Gaku G   Hashimoto-Hachiya Akiko A   Yen Vu Hai VH   Miake Sho S   Takemura Masaki M   Mitamura Yasutaka Y   Ito Takamichi T   Murata Maho M   Furue Masutaka M   Nakahara Takeshi T  

Journal of clinical medicine 20200324 3


<h4>Background</h4>IL-33, one of the IL-1 superfamily cytokines, has been shown to be associated with pruritus and inflammation in atopic dermatitis (AD). Furthermore, IL-33 production derived from keratinocytes reportedly has a crucial role in the development of AD; however, the mechanism of IL-33 expression has not been fully understood.<h4>Methods</h4>We analyzed IL-33 expression in normal human epidermal keratinocytes (NHEKs) treated with IL-4.<h4>Results</h4>IL-4 induced the upregulation of  ...[more]

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