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IL-36γ Inhibits Differentiation and Induces Inflammation of Keratinocyte via Wnt Signaling Pathway in Psoriasis

Wenming Wang, Xiaoling Yu, Chao Wu, Hongzhong Jin

Int J Med Sci. 2017 Aug 18;14(10):1002-1007.

PMID: 28924372

Abstract:

Psoriasis is a common inflammatory skin disease characterized by abnormal keratinocyte inflammation and differentiation that has a major impact on patients' quality of life. IL-36γ, a member of IL-36 cytokine family, is highly expressed in psoriasis and plays an important role in inflammation response and differentiation. However, the function of IL-36γ in differentiation and inflammation of keratinocyte in psoriasis has not been clearly identified. Thus, this study aimed to investigate the role of IL-36γ on differentiation and inflammation in HaCaT cells. HaCaT cells were divided into three groups: (1) Control group; (2) IL-36γ (100 ng/mL) group; (3) IL-36γ (100 ng/mL) + IWP-2 (1μM) group. Real time PCR was used to detect gene expression; the inflammation cytokines were examined by ELISA. We showed that treatment of HaCaT cells with IL-36γ significantly upregulated the expression levels of β-catenin, cyclin D1, and ki-67. IL-36γ also promoted the production of the inflammatory cytokines IFN-γ, IL-1β and IL-6, suppressed the expression of filaggrin, involucrin, keratin 1 and keratin 5. Meanwhile, we demonstrated the role of IWP-2, an inhibitor of the Wnt signaling pathway, in IL-36γ-treated HaCaT cells. Collectively, our findings suggest that IL-36γ inhibits differentiation and induces inflammation of keratinocyte via Wnt signaling pathway in psoriasis, this indicated that downregulation of IL-36γ may be a potential therapeutic option in psoriasis.

Chemicals Related in the Paper:

Catalog Number Product Name Structure CAS Number Price
AP686770616 IWP-2 IWP-2 686770-61-6 Price
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