Chinese Medical Sciences Journal ›› 2019, Vol. 34 ›› Issue (3): 199-204.doi: 10.24920/003489

• Original Article • Previous Articles     Next Articles

IL-36β Promotes Inflammatory Activity and Inhibits Differentiation of Keratinocytes In Vitro

Wang Wenming1, Wu Chao1, Yu Xiaoling2, Jin Hongzhong1, *()   

  1. 1 Department of Dermatology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, China
    2 Department of Dermatology, Dermatology Hospital of Southern Medical University, Guangdong Provincial Dermatology Hospital, Guangdong 510080, China
  • Received:2018-12-28 Published:2019-09-30
  • Contact: Jin Hongzhong

Objective Psoriasis is an immune-mediated inflammatory disease. Despite advances in the study of its pathogenesis, the exact development mechanism of psoriasis remains to be fully elucidated. Hyperproliferative epidermis plays a crucial role in psoriasis. This study aimed to investigate the effects of interleukin-36β (IL-36β) on keratinocyte dysfunction in vitro.

Methods Human keratinocyte cell lines, HaCaT cells, were treated with 0 (control), 50 or 100 ng/ml IL-36β respectively for 24 h. Cell viability was determined with a cell counting kit-8 assay. Flow cytometry was used to assess the effects of IL-36β on apoptosis and cell cycle distribution. Expressions of the differentiation markers, such as keratin 10 and involucrin, were evaluated by quantitative real-time polymerase chain reaction (RT-qPCR). Expressions of the inflammatory cytokines, IL-1β and IL-6 were tested by ELISA.

Results CCK8 assay showed the survival rate had no significant difference between the control and treated group (P > 0.05). Flow cytometry analysis showed cell cycle arrest at S phase in the IL-36β-treated groups compared with the control group (P < 0.05). RT-qPCR verified the decreased mRNA expressions of keratin 10 and involucrin in the IL-36β-treated groups compared with the negative control (P < 0.01). ELISA showed 100 ng/ml IL-36β enhanced levels of IL-1β and IL-6 in culture supernatants of HaCaT cells compared with the negative control (P < 0.05).

Conclusion Taken together, these findings suggest that IL-36β could induce cell cycle arrest at S phase, inhibit keratin 10 and involucrin expressions and promote inflammatory activity in HaCaT cell lines.

Key words: interleukin-36β;, psoriasis, keratinocytes, inflammatory activity, differentiation

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